Autoimmunity And Autoimmune Disease Notes

Autoimmune mechanisms underline many diseases, some organ-specific, others systemic in distribution.

Autoimmune disorders can overlap: an individual may have more than one organspecific disorder;or more than one systemic disease.

Genetic factors such as HLA type are important in autoimmune disease, and it is probable that each disease involves several factors.

Autoimmune mechanisms are pathogenic in experimental and spontaneous animal models associated with the development of autoimmunity.

Human autoantibodies can be directly pathogenic.

Immune complexes are often associated with systemic autoimmune disease.

Autoreactive B and T cells persist in normal subjects but in disease are selected by autoantigen in the production of autoimmune responses.

Microbial cross-reaching antigens and cytokine dysregulation can lead to autoimmunity.

Autoantibody tests are valuable for diagnosis and sometimes for prognosis.

Treatment of organ-specific diseases usually involves metabolic control.
Treatment of systemic diseases includes the use of anti-inflammatory and immunosuppressive drugs.

Future treatment will probably focus on manipulation of the pivotal auto reactive T cells by antigens or peptides, by anti CD4 and possibly T cell vaccination.


The immune system has tremendous diversity and because the repertoire of specificities express by the B- and T-cell populations is generated randomly, it is bound to include many which are specific for self components. Thus the body must establish self-tolerance mechanisms, to distinguish between self and non-self determinants, so as to avoid auto reactivity (see Chapter 7). However, al mechanism has a risk of breakdown. The self recognition mechanisms are no exception, and a number of disease have been identified in which there is autoimmunity, due to copious production of autoantibodies and auto reactive T cells. One of the earliest examples in which the production of autoantibodies was associated with disease in a given organ is Hashimoto’s thyroiditis. Among the autoimmune diseases, thyroiditis has been particularly well-studied, and many of the aspects discussed in this chapter will draw upon our knowledge of it. It is a disease of the thyroid which is most common in middle-aged women and often lead to formation of a goiter and hypothyroidism.

The gland is infiltrated, sometimes to an extraordinary extent, with inflammatory lymphoid cells.

These are predominantly mononuclear phagocytes, lymphocytes and plasma cells, and secondary lymphoid follicles are common (Figure-1). In Hashimoto’s disease, the gland often shows regenerating thyroid follicles but this is not a feature of the thyroid in the related condition, primary myxoedema, in which comparable immunology features are seen and where the gland undergoes
almost complete destruction and shrinks. The serum of patients with Hashimoto’s disease usually contains antibodies to thyroglobulin. These antibodies are demonstrable by agglutination and by precipitin reactions when present in high titre. Most patients also have anti bodies directed against a
cytoplasmic or microsome antigen, also present on the apical surface of the follicular epithelial cells (Figure-2), and now known to be thyroid peroxidase, the enzyme which iodinates thyroglobulin.


The antibodies associated with Hashimoto’s thyroiditis and primary myxoedema react only with the thyroid, so the resulting lesion is highly localized. By contrast, the serum from patients with diseases such as systemic lupus crythematosus (SLE) reacts with many, if not all, of the tissues I the body. In SLE, one of the dominant antibodies is directed against the cell nucleus (Figure-2). These two diseases represent the extremes of the autoimmune spectrum (Figure-3). The common target organs in organ-specific disease include the thyroid, adrenals, stomach and pancreas. The non-organ-specific diseases, which include the rheumatological disorders, characteristically involve the skin, kidney, joints and muscle (Figure-4).

An individual may have more then one autoimmune disease

Interestingly, there are remarkable overlaps at each end of the spectrum. Thyroid antibodies occur with a high frequency in pernicious anaemia patients who have gastric autoimmunity, and these patients have a higher incidence of thyroid autoimmune disease than the normal population.

Similarly, patients with thyroid autoimmunity have a high incidence of stomach autoantibodies and, to a lesser extent, the clinical disease itself, namely pernicious anaemia. The cluster of hematological disorders at the other end of the spectrum also shows considerable overlap. Features of rheumatoid
arthritis, for example, are often associated with the clinical picture of SLE. In these diseases immune complexes are deposited systemically, particularly in the kidney, joints and skin, giving rise to widespread lesions. By contrast, overlap of diseases from the two ends of the spectrum is relatively
rare. The mechanisms of immunopathological damage vary depending on where the disease lies in the spectrum. Where the antigen is localized in a particular organ, Type II hypersensitivity and cell-mediated reactions are most important. In non-organ-specific autoimmunity, immune complex deposition leads to inflammation through a variety of mechanisms, including complement activation and phagocyte recruitment.


Autoimmune disease can occur in families

There is an undoubted family incidence of autoimmunity. This is largely genetic rather than environmental, as many be seen from studies of identical and non-identical twins, and from the associated of thyroid autoantibodies with abnormalities of the Xchromosome. Within the families of patients with organ-specific autoimmunity, not only is there a general predisposition to develop organ-specific antibodies, it is also clear that other genetically controlled
factors tend to select the organ that is mainly affected. Thus, although relatives of Hashimoto patients and families of pernicious anaemia patients both have higher than normal incidence and titer of thyroid autoantibodies, the relatives of pernicious anaemia patients have a far higher frequency of gastric autoantibodies, indicating that there are genetic factors which differentially
select the stomach as the target within these families.

Certain HLA Haplotypes Predispose To Autoimmunity

Further evidence for the operation of genetic factors in autoimmune disease comes from their tendency to be associated with particular HLA specificities (Figure-5). Rheumatoid arthritis shows no associations with the HLA-A and-B loci haplotypes, but is associated with a nucleotide sequence (encoding amino
acids 70-74 in the DRβ chain) that is common to DR1 and major subtypes of DR4.

This sequence is also present in the dnaJ heat-shock proteins of various bacilli and EBV gp 110 proteins, presenting an interesting possibility for the induction of autoimmunity by a microbial cross-reacting epitope (see below). The plot gets even deeper, though, with the realization that HLA-DR molecules bearing this sequence can bind to another bacterial heat shock protein, dna K, and to the human analogue, namely hsp73, which targets selected proteins to lysosomes for antigen processing. The haplotype B8, DR3 is particularly common in the organ specific diseases, although Hashimoto’s thyroiditis tends to be associated more with DR5. It is notable that for insulin-dependent (type 1) diabetics mellitus, DQ2/8 heterozygotes have a greatly increased risk of
developing the disease (Figure-5). Although HLA risk factors tend to dominate-wide searches for mapping the genetic intervals containing genes for predisposition to disease by linkage to micro satellite markers (polymorphic variable numbers of tandem repeats, VNTR) reveal a plethora of genes affecting loss of tolerance, sustained inflammatory responses and end-organ targeting.


Autoimmune processes are often pathogenic. When autoantibodies are fond in association with a particular disease there are three possible inferences:
• The autoimmunity is responsible for producing the lesions of the disease.

• There is a disease process which, through the production of tissue damage, leads to the development of autoantibodies.

• There is a factor which produces both the lesions and the autoimmunity. Autoantibodies secondary to a lesion (the second possibility) are sometimes found. For example, cardiac autoantibodies may develop after myocardial infarction. However, sustained production of autoantibodies rarely follows the release of autoantigens by simple trauma. In most diseases associated with autoimmunity, the evidence supports the first possibility, that the autoimmune
process produces the lesions.

The pathogenic role of autoimmunity can be demonstrated in experimental models

Examples of induced autoimmunity

The most direct test of whether autoimmunity is responsible for the lesions of disease is to induced autoimmunity deliberately in an experimental animal and see if this leads to the production of the lesions. Autoimmunity can be induced in experimental animals by injecting auto antigen (self antigen) together with complete Freund’s adjuvant, and this does indeed produce organ-specific
disease in certain organs. For example, thyroglobulin injection can induce an inflammatory disease of the thyroid while myelin basic protein can cause encephalomyelitis. In the case of thyroglobulin-injected animals, not only are thyroid autoantibodies produced, but the gland becomes infiltrated with mononuclear cells and the acinar architecture crumbles, closely resembling the histology of Hashimoto’s thyroiditis. The ability to induce experimental autoimmune disease depends on the strain of animal used.

For example, it is found that the susceptibility of rats and mice to myelin basic protein-induced encephalomyelitis depends on a small number of gene loci, of which the most important are the MHC class II genes. The disease can be induced in susceptible strains by injecting T cells belong to the CD4/TH1 subset and it has been found that induction of disease can be prevented by treating
the recipients with antibody to CD4 just before the expected time of disease onset, blocking the interaction of the TH cells’ CD4 with the class II MHC of antigen-presenting target cells. The results indicate the importance of class II restricted auto reactive TH cells I the development of these conditions, and emphasize the prominent role of the MHC.

Examples of spontaneous autoimmunity

It has proved possible to breed strains to animals which are genetically programmed to develop autoimmune diseases closely resembling their human counterparts. One well established example is the Obese strain (OS) chicken (Figure-6) which parallels human autoimmune thyroid disease in terms
of the lesion in the gland, the production of antibodies to different components in the thyroid, and the overlap with gastric autoimmunity. So it is of interest that when the immunological status of these animals is altered, quite dramatic effects on the outcome of the disease are seen.

For example, removal of the thymus at birth appears to exacerbate the thyroiditis, suggesting that the thymus exerts a controlling effect on the disease, but if the entire T-cell population is abrogated by combining thymectomy with massive injections of anti-chick T-cell serum, both autoantibody production and the attack on thyroid are completely inhibited. Thus, T cells play a variety of pivotal roles as mediators and regulators of this disease. The non-obese diabetic (NOD) mouse provides an excellent model for human insulin-dependent diabetes mellitus (IDDM; type 1 diabetes) where the
insulin producing β cells of the pancreatic islets of Langerhans are under attack from a chronic leukocytic infiltrate of T cells and macrophages (Figure-7). The role of the T cells in mediating this attack is evident from the amelioration and prevention of disease by treatment of the mice with a non-depending anti-CD4 monoclonal antibody, which in the presence of the pancreatic auto-antigens, insulin and glutamic acid decarboxylase (GAD) induces specific T cell anergy.
The dependence of yet another spontaneous model, the F1 hybrid of New Zealand Black and White strains (NZB x W/F1), on the operation of immunological processes is aptly revealed by the suppression of the murine SLE which characterizes this strain, by treatment with anti-CD4 (Figure-8).

Human autoantibodies can be directly pathogenic

When investigating human autoimmunity directly, rather than using animal models, it is of course more difficult to carry out experiments. Nevertheless, there is much evidence to suggest that autoantibodies may be important in pathogenesis, and we will discuss the major examples here.

Thyroid autoimmune disease – A number of disease have been recognized in which autoantibodies to hormone receptors may actually mimic the function of the normal hormone concerned and produce disease. Graves’ disease (thyrotoxicosis) was the first disorder in which such anti-receptor antibodies were clearly recognized. The phenomenon of neonatal thyrotoxicosis provides us with a natural ‘passive transfer’ study, because the IgG antibodies from the thyrotoxic mother cross the placenta and react directly with thyroid stimulating hormone (TSH) receptor o the neonatal thyroid.

Many babies born to thyrotoxic mothers and showing thyroid hyperactivity have been reported, but the problem spontaneously resolves as the antibodies derived from the mother are catabolized in the baby over several weeks. Whereas autoantibodies to the TSH receptor may stimulate cell division and/or increase the production of thyroid hormones, others can bring about the opposite effect by inhibiting these functions, a phenomenon frequently observed in the receptor responses to ligands which act as agonists or antagonists. Different combinations of the various manifestations of
thyroid autoimmune disease, chronic inflammatory cell destruction and stimulation or inhibition of growth and thyroid hormone synthesis, can give rise to a wide spectrum of clinical thyroid dysfunction (Figure-9).

Myasthenia gravis – A parallel with neonatal hyperthyroidism has been observed with mothers suffering from myasthenia gravis, where antibodies to acetylcholine receptors cross the placenta into the fetus and may cause transient muscle weakness in the newborn baby.

Other receptor diseases – Somewhat rarely, autoantibodies to insulin receptors and to βadrenergic receptors can be found, the latter associated with bronchial asthma. Neuromuscular defects can be elicited in mice injected with serum from patients with the Lambert – Eaton syndrome containing antibodies to presynaptic calcium channels, while sodium channel autoantibodies have been identified in the Guillain – Barre syndrome.

Male infertility – Yet another example of autoimmune disease is seen in rate cases of male infertility were antibodies to spermatozoa lead to clumping of spermatozoa, either by their heads or by their tails, in the semen.

Pernicious anaemia – In this disease an autoantibody interferes with the normal uptake of vitamin B12.Vitamine B12 is not absorbed directly, but must first associated with a protein called intrinsic factor; the vitamin-protein complex is then transported across the intestinal mucosa. Early passive transfer studies demonstrated that serum from a patient with pernicious anaemia, if fed to a healthy individual together with intrinsic factor – B12 complex, inhibited uptake of the vitamin.

Subsequently, the factor in the serum which blocked vitamin uptake was identified as antibody against intrinsic factor. It is now known that plasma cells in the gastric mucosa of patients with pernicious anaemia secrete this antibody into the lumen of the stomach (Figure-10).

Goodpasture’s syndrome – In goodpasture’s syndrome, antibodies to the glomerular capillary basement membrane bind to the kidney in vivo (Figure-3). To demonstrate that the antibodies can have a pathological effect, a passive transfer experiment was performed. The antibodies were eluted from the kidney of a patient who had died with this disease, and injected into primates whose kidney antigens were sufficiently similar for the injected antibodies to localize on the glomerular basement membrane. The injected monkeys subsequently died with glomerulonephritis.

Blood and vascular disorders – Autoimmune haemolytic anaemia and idiopathic thrombocytopenia purpura result from the synthesis of autoantibodies to red cells and platelets, respectively. The
primary antiphospholipid syndrome characterized by recurrent thromboembolic phenomena and feta loss is triggered by the reaction of autoantibodies with a complex of β2-glycoprotein turns up again as an abundant component of atherosclerotic plaques and there is increasing attention to the idea that autoimmunity may initiate or exacerbate the process of lipid deposition and plaque formation in this disease, the two lead candidate antigens being heat-shock protein 60 and the low- density lipoprotein, apoprotein B. The necrotizing granulomatous vasculitis which characterizes
Wegener’s granulomatosis is associated with antibodies to neutrophil cytoplasmic proteinase III (cANCA) but their role in pathogenesis of the vaculitis is ill defined.

Immune Complexes appear to be pathogenic in systemic autoimmunity

In the case of SLE, it can be shown that complement-fixing complexes of antibody with DNA and other nucleosome components such as histones are deposited in the kidney (Figure-3), skin, joints and choroid plexus of patients, and must be presumed to produce Type III hypersensitivity reactions.
Cationic anti-DNA antibodies and histones facilitate the binding to heparin sulphate in the connective tissue structures. Individuals with genetic deficiency of the early classical pathway complement components clear circulating immune complexes very poorly and are unduly susceptible to the development of SLE. Turing to the experimental models, we have already mentioned the (NZB x W) F1 which spontaneously develops murine SLE associated with immune-complex glomerulonephritis and anti-DNA autoantibodies as major features. The fact that measures which suppress the immune response in these animals (e.g. treatment with azathioprine or anit-CD4) also suppress the disease and prolong survival, adds to the evidence for autoimmune reactions causing such disease (Figure-8).

The erosions of cartilage and bone in rheumatoid arthritis are mediated by macrophages and fibroblasts which become stimulated by cytokines from activated T cells and immune complexes generated by a vigorous immunological reaction within the synovial tissue. The complexes can arise
through the self-association of IgG rheumatoid factors specific for the Fcy domains, a process facilitated by the striking deficiency of terminal galactose on the biantennary N-linked Fc iligosaccharides (Figure-11). This agalacto glycoform of IgG in complexes can exacerbate inflammatory reactions through reaction with mannosebinding lectin and production of TNE.

Evidence for directly pathogenic T cells in human autoimmune disease is hard to get

Adoptive transfer studies have shown that TH1 cells are responsible for directly initiating the lesions in experimental models of organ-specific autoimmunity. In the human, the production of high affinity, somatically mutated IgG autoantibodies characteristic of Tdependent responses, the isolation of thyroid-specific T-cell clones from the glands of Graves’ disease patients, the beneficial effect of cyclosporine in pre-diabetic individuals and the close association with certain HLA haplotypes, make it abundantly clear that T cells are utterly pivotal for the development of autoimmune disease. However, it is difficult to identify a role for the T cell as a pathogenic agent as
distinct from a T-helper function in the organ-specific disorders. Indirect evidence from circumstances showing that antibodies themselves do not cause disease, such as in babies born to mothers with insulin-dependent diabetes (IDDM), may be indicative.

Autoimmunity is antigen driven

Given that auto-reactive B cells exist, the question remains whether they are stimulated to proliferate and produce autoantibodies by interaction with auto-antigens or by some other means, such as non-specific polyclonal activators or idiotypic interactions (Figure-14). Evidence that B cells are selected by antigen comes from the existence of high affinity autoantibodies which arise through
somatic mutation, a process which requires both T cells and autoantigen.

Additionally, autoantibodies to epitope clusters occur on the same auto-antigenic molecule. Apart from the presence of auto-antigen itself, it is very difficult to envisage a mechanism that could account for the co-existence of antibody responses to different epitopes on the same molecule. A similar argument applies to the induction, in a single individual, of autoantibodies to organcelles (e.g. nucleosomes and spliceosomes which appear as belbs on the surface of apoptotic cells) or antigens linked within the same organ (e.g. thyroglobulin and thyroid peroxidase).

The most direct evidence for autoimmunity being antigen driven comes from studies of the Obese strain chicken which, as described earlier, spontaneously develops thyroid autoimmunity. If the thyroid gland (the source of antigen) is removed at birth, the chickens mature without developing
thyroid autoantibodies (Figure-13). Furthermore, once thyroid autoimmunity has developed, later removal of the thyroid leads to a gross decline of thyroid autoantibodies, usually to undetectable levels. Comparable experiments have been carried out in the non-obese diabetic (NOD) mouse which models human autoimmune diabetes; chemical destruction of the β cells leads to decline in
pancreatic autoantibodies. DNase treatment of lupus mice ameliorates the disease, presumably by destroying potentially pathogenic immune complexes.

In organ-specific disorders, there is ample evidence for T cells responding to antigens present in the organs under attack. But in non-organ-specific autoimmunity, identification of the antigens recognized by T cells is often inadequate. True, histone-specific T cells are generated in SLE patients
and histone could pay a ‘piggy back’ role in the formation of anti-DNA antibodies by substituting for natural antibody in the mechanism outlined in Figure-14. Another possibility is that the T cells do not see conventional peptide antigen (possibly true of anit-DNA responses) but instead recognize an
antibody’s idiotype (an antigenic determinant on the V region of antibody). In this view SLE, for example, might sometimes be initiated as an ‘idiotype disease’, like the model presented in Figure-14 In this scheme, autoantibodies are produced normally at low levels by B cells using germ-line genes. If these then form complexes with the autoantigen, the complexes can be taken up by APCs (including B cells) and components of the complex, including the antibody idiotype, presented to T cells. Idiotype-specific T cells would then help the autoantibody-producing B cells. Evidence for the induction of anti-DNA and glomerulonephritis by immunization of mice with the idiotype of germ-line ‘natural’ antiDNA autoantibody lends credence to this hypothesis.

Controls on the development of autoimmunity can be bypassed in a number of ways

Molecular mimicry by cross-reactive microbial antigens can stimulate autoreactive B and T cells

Normally, naïve autoreactive T cells recognizing cryptic self epitopes are not switched on because the antigen is only presented at low concentrations on ‘professional’ APCs or it may bepresented on ‘non-professional’ APCs such as pancreatic β-islet cells or thyroid epithelial cells, which lack B7 or other co-stimulator molecules. However, infection with a microbe bearing antigens that cross-react with the cryptic self epitopes (i.e. have shared epitopes) will load the professional APCs with levels of processed peptides that are sufficient to activate the naïve autoreactive T cells. Once primed, these T cells are able to recognize and react with the self epitope on the non-professional APCs since they no longer require a co-stimulatory signal and have a higher avidity for the target, due to upregulationof accessory adhesion molecules (Figure-15). 

Cross reactive antigens which share B cell epitopes with self molecules can also break tolerance but by a different mechanism. Many autoreactive B cells cannot be activated because the CD4+ helper T cells which they need are unresponsive either because these helper T cells are tolerized at lower concentration of autoantigens than the B cells or because they only recognize cryptic epitopes. However, these ‘helpless’ B cells can be stimulated if the cross-reaching antigen bears a ‘foreign’ carrier epitope to which the T cells have not been tolerized (Figure-16). The autoimmune process may persist after clearance of the foreign antigen if the activated B cells now focus the autoantigen on their surface receptors and present it to normally resting autoreactive T cell which will then proliferate and act as helpers for fresh B-cell stimulation.

A disease in which such molecular mimicry operates is rheumatic fever, in which autoantibodies to heart valve antigen can be detected. These develop in a small proportion of individuals several weeks after a streptococcal infection of the throat. Carbohydrate antigens on the streptococci cross-react with an antigen on heart valves, so the infection may bypass T-cell self tolerance to heart valve antigens. Shared B-cell epitopes between Yersinia enterolytica and the extracellular domain of the TSH receptor have recently been described. There may also be cross reactivity between HLA-B27 and certain strains of Klebsiella in connection with ankylosing spondylitis, and crossreactivity between bacterial heat-shock proteins and DR4 in relationship to rheumatoid arthritis. 

In this connection, it has been suggested that because processed MHC molecules may represent a major fraction of the peptide emitopes presented to differentiating T cells within the thymus, a significant proportion of positively selected cell which escape negative selection and enter the periphery will be specific for weakly binding cryptic MHC epitopes. One might therefore expect autoimmune responses to arise not infrequently through activation of these cells by molecular mimicry.

In some cases foreign antigen can directly stimulate auto-reactive cells 

Another mechanism to bypass the tolerant autoreactive TH cell is where antigen or another stimulator directly triggers the autoreactive effector cells. For example, lipopolysaccharide or Epstein-Barr virus causes direct B-cell stimulation and some of the clones of activated cells will produce autoantibodies, although in the absence of T-cell help these are normally of low titer and affinity. However, it is conceivable that an activated B cell might pick up and process its cognate autoantigen and present it to a naïve autoreactive T cell. 

Cytokine dysregulation, inappropriate MHC expression and failure of suppression may induce autoimmunity 

It appears that dysregulation of the cytokine network can also lead to activation of autoreactive T cells. One experimental demonstration of this is the introduction of a transgene for interferon-γ (IFNγ) into pancreatic β-islet cells. If the transgene for IFNγ is fully expressed in the cells, MHC class II genes are upregulated and autoimmune destruction of the islet cell results (Figure-17). This is not simply a result of a nonspecific chaotic IFNγ-induced local inflammatory milieu since normal islets grafted at a separate site are rejected, implying clearly that T-cell autoreactivity to the pancreas has been established.

The surface expression of MHC class II in itself is not sufficient to activate the naïve autoreactive T cells but it may be necessary to allow a cell to act as a target for the primed autoreactive TH cells, and it was therefore most exciting when cells taken from the glands of patients with Graves’ disease were found to be actively synthesizing class II MHC molecules (Figure-18) and so were able to be recognized by CD4+ T cells. In this context it is interesting that isolated cells from several animal strains that are susceptible to autoimmunity are also more readily induced by IFNγ to express MHC class II than are cells from non-susceptible strains. 

The argument that imbalanced cytokine production may also contribute to autoimmunity receives further support from the unexpected finding that tumour necrosis factor (introduced by means of a TNF transgene) ameliorates autoimmune disease in NZB x NZW hybrid mice. 

Aside from the normal ‘ignorance’ of cryptic self-epitopes, other factors which normally restrain potentially autoreactive cells may include regulatory T cells, hormones (e.g. steroids), cytokines (e.g. TGFβ) and products of macrophages (Figure-19). Deficiencies in any of them may increase susceptibility to autoimmunity. The feedback loop on Thelpersand macrophages through the pituitary – adrental axis is particularly interesting, as defects at different stages in the loop turn up in a variety of autoimmune disorders Figure-20). For example, patients with rheumatoid arthritis have low circulating corticosteroid levels compared with controls, and after surgery, although they produce copious amounts of IL-1 

and IL-6, a defect in the hypothalamic paraventricular nucleus prevents the expected increase in ACTH and adrenal steroid output. A subset of CD4 regulatory cell present in young healthy mice of the NOD strain can prevent the transfer of disease by spleen cells of diabetic animals to NOD mice congenic for the severe combined immunodeficiency trait; this regulatory subset is lost in older mice.

Pre-existing defects in the target organ may increase susceptibility to autoimmunity

We have already alluded to the undue sensitivity of target cells to upregulation of MHC class II by IFNγ in animals susceptible to certain autoimmune disease: Other evidence also favours the view that there may be a pre-existing defect in the target organ. In the Obese strain chicken model of spontaneous thyroid autoimmunity, not only is there a low threshold of IFNγ induction of MHC class II expressin by thyrocytes but it has also been shown that, when endogenous TSH is suppressed by thyroxine treatment, the uptake of iodine into the thyroid glands is far higher in the Obese strain than in a variety of normal strains. Furthermore, this is not due to any stimulating animals show even higher uptakes of iodine (Figure-21). Interestingly, the Cornell strain (from which the Obese strain was derived by breeding) shows even higher uptakes of iodine, yet these animals do not develop spontaneous thyroiditis. This could be indicative of a type of abnormal thyroid behavior which in itself is insufficient to induce autoimmune disease but does contribute to susceptibility in the Obese strain. Other situations in which the production of autoantigen is affected are diabetes, in which one of the genetic risk factors is associated with a microsatellite marker lying within a transcription factor controlling the rate of insulin production, and rheumatoid arthritis, in which the agalacto IgG glycoform is abnormally abundant. The intriguing observations that immunization atherosclerotic lesions at classical predilection sites object to major haemodynamic stress and that patients with atherosclerosis produce antibodies to human hsp60 which react with heat or IFNα-stressed endothelial cells, hints strongly at an autoimmune contribution to the pathology of the disease. Particularly relevant to the present discussion is the finding of upregulated hasp60 expression at such critical sites even in a 5-month-old child (Figure22). Again, one must re-emphasize the considerable importance of multiple factors I the establishment of prolonged autoimmunity.


Wherever the relationship of autoantibodies to the disease process, they frequently provide valuable markers for diagnostic purposes. A particularly good example is the test for mitochondrial antibodies, used in diagnosing primary biliary cirrhosis (Figure-23). Exploratory laparotomy was previously needed to obtain this diagnosis, and was often hazardous because of the age and condition of the patients concerned. Autoantibodies often have predictive value. For instance, individuals testing positively for antibodies to both insulin and glutamic acid decarboxylase have a high risk of developing insulin-dependent diabetes.


Often, in organ-specific autoimmune disorders, the symptoms can be conrolled by administration of thyroxine, and thyrotoxicosis by antithyroid drugs. In pernicious anaemia, 

metabolic correction is achieved by injection of vitamin B12, and in myasthenia gravis by administration of cholinesterase inhibitors. If the target organ is not completely destroyed, it may be possible to protect the surviving cells by transfection with FasL or TGFβ genes. Where function is completely lost and cannot be substituted by hormones, as many occur in lupus nephritis or chronic rheumatoid arthritis, tissue grafts or mechanical substitutes may be appropriate. In the case of tissue grafts, protection from the immunological processes which necessitated the transplant may be required.

Conventional immunosuppressive therapy with antimitotic drugs at high doses can be used to dam down the immune response but, because of the dangers involved, tends to be used only in life-threatening disorders such as SLE and dermatomyositis. The potential of cyclosporine and related drugs such as rapamycin has yet to be fully realized, but quite dramatic results have been reported in the treatment of type 1 diabetes mellitus. Anitinflammatory drugs are, of course, prescribed for rheumatoid diseases with the introduction of selective cyclo-oxygenase-2 (COX-2) inhibitors representing a welcome development. Encouraging results are being obtained by treatment of rheumatoid arthritis patients with low steroid doses at an early stage to correct the apparently defective production of these corticosteroids by the adrenal feedback loop, and for those with more established disease, attention is now focused on the striking remissions achieved by synergistic treatment with anti-TNFα monoclonals plus methotrexate.

As we understand more about the precise defects, and learn how to manipulate the immunological status of the patient, some less well-established approaches may become practicable (Figure-24). Several centres are trying out autologous stem-cell transplantation following haemato-immunoablation with cytotoxic drugs in severe cases of SLE, scleroderma and rheumatoid arthritis. Draconian reduction in the T cells in multiple sclerosis by Campath-1H (anti-CD52) and of the B-cell population with antiCD20 in rheumatoid arthritis are both under scrutiny. Treatment with Campath-1H followed by a non-depleting anti-CD4 has produced excellent remissions in patients with Wegener’s granulomatosis who were refractory to normal treatment. In an attempt to establish antigenspecific suppression, considerable clinical improvement has been achieved in exacerbating remitting multiple sclerosis by repeated injection of Cop 1, a random copolymer of alanine, glutamic acid, lysine and tyrosine meant to simulate the postulated ‘guilty’ autoantigen, myelin basic protection. Some experimental autoimmune disease have been treated successfully by feeding antigen to induce oral tolerance, by the inhalation of autoantigenic peptides and their analogues (Figure-25), and by ‘vaccination’ with peptides from heat-shock protein 70 or the antigen-specific receptor or autoreactive T cells. This suggests that stimulating normally suppressive functions, including the idiotype network, could be promising.

CRITICAL THINKING: Autoimmunity and autoimmune disease

Miss Jacob, a 30-year-old Caribbean lady, was seen in a rheumatology clinic with stiff painful joints in her hands, which were worse first thing in the morning. Other symptoms included fatigue, a low-grade fever, a weight loss of 2 kg, and some mild chest pain. Miss Jacob had recently returned to the UK from a holiday in Jamaica and was also noted to be taking the combined oral contraceptive pill. Past medical history of note was a mild autoimmune haemolytic anaemia 2 years previously. On examination Miss Jacob had a non-specific maculopapular rash on her face and chest and patchy alopecia (hair loss) over her scalp. Her mouth was tender and examination revealed an ulcer on the soft palate. She had moderately swollen and tender proximal interphalangeal joints. Her other joints were unaffected, but she had generalized muscle aches. The results of investigations are shown in Figure-26.

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When writing a biological research paper, you should use scholarly sources. While there is a lot of misinformation on the internet, it’s best to stick to academic essay writing service to get the most accurate information. Most libraries allow you to select a peer-review filter that will restrict your search results to academic journals. It’s also helpful to be familiar with the differences between scholarly and popular sources.

Using statistical tests

Using statistical tests when writing a biological paper requires that you make certain assumptions about the results you are describing. The most common statistical tests are parametric tests that are based on assumptions about conditions or parameters. About 22% of the papers in our review reported violations of these assumptions, and such violations can lead to inappropriate or invalid conclusions.

Statistical tests are important in biological research because they allow researchers to determine if their data is statistically significant or not. The power of these tests depends on the size of the dataset. Larger datasets produce more significant results. The power of these tests also depends on the assumption of independence between measurements. This is important because the results can be different if there are duplications or different levels of replications.

Hypothesis tests are useful in evaluating experimental data. They identify differences and patterns in data. They are useful tools for structuring biological research.

Avoiding hedge words

Hedge words are phrases or words used to express uncertainty in a scientific paper. They can help writers avoid making inaccurate claims while still being respectful of the reader’s opinion. However, writers must be careful to avoid using too many hedges. 

Listed below are a few guidelines to help you avoid these words:

  • Hedge words shift the burden of responsibility from the writer to the reader. 
  • Hedge words can be a sign of uncertainty or overstatement. They can also be used to limit the scope of an assertion. They also convey an opinion or hypothesis. When choosing a hedging strategy, be careful not to use words such as “no data” or “unreliable.” These words can convey a degree of uncertainty and imply that the findings cannot be confirmed.

The use of hedge words is common in academic writing. However, they hurt your audience. It is a linguistic strategy that writers use as a way to reassure readers. The goal is to guide readers and make them feel comfortable with the idea that the author does not know all the answers.

Choosing a format

Biological research papers have different formats, and you should choose one that suits the nature of your paper. It should be based on credible and peer-reviewed sources. The best sources to use for biology papers are books, specialized journals, and databases. Avoid personal blogs, social networks, and internet discussions, as these are not suitable for a research paper.

Biology research papers focus on a specific issue and present different arguments in support of a thesis. Traditionally, they are based on peer-reviewed sources, but you can also conduct your independent research and present unique findings. Biology is a complex field of study. The subject matter varies, from the basic structure of living things to the functions of different organs. It also explores the process of evolution and the life span of different species.

Formatting your bibliography

When writing a biological research paper, the format of your bibliography is crucial. It should follow a standardized citation style such as the “Author, Date” scientific style. The format should be arranged alphabetically by author, and you should use numbered references to indicate key sources.

Reference lists must be comprehensive and contain enough information to enable readers to find the sources themselves. Although the format is not as important as completeness, it can help readers quickly identify the authors and sources. Bibliographies are usually reverse-indented to make them easier to find.

In-text citations should include the author’s last name, preferred name, and the page number. Usually, authors do not separate their surname and year of publication. In addition, you should also include the location, which is usually the publisher’s office.

If a work has more than four authors, you should list up to ten in the reference list. The first author’s surname should be used, followed by “et al.” Likewise, you should list more than ten authors in the reference list.

When writing a biological research paper, it is important to ensure that your bibliography is formatted properly. When you write the title, you should use boldface and uppercase letters. The title should also be focused, not too long or too short. It should take one or two lines and all text should be double-spaced. You should also type the author’s name after the title. Don’t forget to indicate the location of your research as well as the date you submitted the paper.

How to Learn Biology in a Fun Way

Biology is a vast area of study and a good way to get students interested through an introduction to the subject. A good introduction to the topic should include the basics and include activities that encourage exploration. For example, let students try magnifying cells, bacteria, and other things using microscopes. Introduce the student to the field of biology with easy activities and fun questions. Include topics such as botany, anatomy, physiology, and zoology.

Biology is a practical science and learning about biological systems through experiments in a lab will help students understand concepts and retain information. Students will remember a lesson that takes place in a lab setting much longer than in a textbook. They’ll be more interested in biology, and the material will stick with them more.

One of the best ways to remember what you’ve learned is to apply it to other people. This will help you to move information from your short-term memory to your long-term memory. Another great way to get biology concepts stuck in your brain is to teach them to other people. This method allows you to review what you’ve learned with your classmate.

Introducing Experiments into the Curriculum

Biology experiments are a great way to help students learn the fundamentals of biology. This type of course also allows students to apply their learning to other subjects. By incorporating experiments into the biology curriculum, students can learn more about different organisms and their behavior. Students who enjoy science and want to learn more about it should consider incorporating experiments into their courses.

Throughout the curriculum, students will learn about principles governing ecosystems, communities, and populations. If student have a college task to write about biology and don’t have enough time, they can request a help from coursework writer and get well written essay. They will also learn about the structure and function of nucleic acids and how these can affect our lives. They will also learn about the functions of the human genome and how genes are passed from generation to generation.

Undergraduate students studying biology should be exposed to more physical sciences and mathematics. Currently, undergraduate students are not taught these fundamentals. They need a strong background in these subjects to be able to understand contemporary biology. Most universities offer courses in all areas of the physical sciences, and these courses may be able to help students master the basic concepts they need to understand contemporary biology.

Use a Variety of Instructional Materials

Biology is an exciting subject to teach, and it can appeal to students of all ages. However, if you want your students to retain information, you must use innovative teaching methods. Dry lectures and reading textbooks will not spark much interest in students. The best way to engage students in this subject is to combine various materials. Incorporating hands-on learning opportunities is essential for biology students, and this approach will boost retention.

One of the helpful resource for biology educators is the iBiology Scientific Teaching Series. This collection of educational videos and tutorials is an excellent source for undergraduate biology instructors. These resources also emphasize evidence-based pedagogy and active learning. In addition to the iBiology Scientific Teaching Series, you can also utilize CourseSource, an open-access journal of peer-reviewed teaching resources. These resources are organized around course units in biology and aligned with the learning objectives set by professional societies.

Explain to Students what Biology is for

Biology isn’t the easiest subject to teach, but there are some creative ways to make it fun for students. For example, you can read a book about the life of a bacterium or explain the role of chromosomes. You can also discuss how organisms use energy and matter to survive. Afterward, you can discuss how DNA codes and chromosomes can affect the characteristics of offspring. In addition, you can talk about how genetic counseling and biotechnology can help humans.

One way to explain to students what biology is is to show them a diagram of DNA and how it works. DNA is a molecule made up of two strands that coil and twist to form a double helix. Each strand contains hundreds of thousands or millions of base pairs. In eukaryotic cells, DNA coils around proteins called histones to form a nucleosome.

Another great way to motivate students to engage with biology is to use stories. Stories are memorable and easy to understand, so students are more likely to remember them. Another effective way to make biology fun is to use 3D lab simulations like Labster, which follow a storyline.

One great way to explain to students what biology is for is to highlight its relevance to everyday life. In this way, students can relate biology to their everyday lives, which can influence their career choices. 

Discuss what You’ve already Learned

Whether you’re taking a biology course in college or just want to earn credits to get into medical school, you can learn how to earn biology in a fun way. Instead of boring lectures and tests, try to make the course more engaging by using a variety of creative teaching techniques. For example, consider using stories to introduce topics. Not only are they easy to remember, but they are also fun! One way to use stories in biology courses is through Labster simulations, which follow a storyline.

Explaining what you’ve learned to a classmate will help you recall concepts better, which will help you retain the information in your long-term memory. Also, remember that biology is full of specialized vocabulary. To learn this vocabulary, you can discuss it with a classmate and use it in sentences.


Getting the right feedback can help you improve your work. It’s important to get feedback from your peers and instructors. This way, you can learn from their strengths and weaknesses. Then, you can improve your conclusions. Use the “So what?” Game to help you refine your conclusion.

A good thesis conclusion should be memorable. It could include a call-to-action, a recommendation, or a note about future research. It should also refer back to the introduction, and use some keywords from the introduction. This will help your reader feel that they have learned something from your essay and are ready to take action.

How to Write an Excellent Biology Research Paper

A good example of a biology research paper is not hard to find. The trick, however, is not to find it, but to understand how it was created. Writing such an assignment requires precision, dedication, and an understanding of the rules and expectations of such a paper. And many students are forced to seek biology homework help from various homework help websites like and many others. So, here is a quick guide on how to write a biology research paper. Read, learn, apply, and enjoy the results!

Choose a Topic

Before considering other questions, such as what methods are best to use, asking for paper writing helpfrom an essay helper, or how to format a biology research paper, you need to choose a topic.A title or a thesis statement are not the same as a topic. You choose a general theme for your paper by selecting a topic. It ought to be limited enough to maintain a focused objective. But it shouldn’t be overly constrained. If not, it will be difficult for you to do research and locate the needed sources. Our recommendation applies to selecting a topic for research papers on human resources, technology, or history as well. Pick something you are already familiar with to investigate it more thoroughly.

Thesis Statement Definition

The thesis statement is what you can write once you have your topic selected. A thesis statement encapsulates your work’s definition and main goal. Here, you describe the goal of your research—what you hope to learn, demonstrate, or test. You present reasons for why your research is important and what results you want to achieve from the assigned assignment.

You will never find a biology research paper example without a clear thesis statement in the work’s introduction. You must follow these examples and briefly state your work’s goal in the final paragraph of your introduction. The two key components of any introduction are the thesis statement and the overarching theme of your work.


The logical next step for you is to conduct research on your subject. It’s best to finish this step before beginning the outlining process. Make sure your study has application in your field throughout this phase. In other words, you should check to determine if other researchers have conducted similar studies and if you have any original research to offer. If you can’t, you should probably switch topics.

Additionally, you should try to locate all the resources you’ll need to do your assignment during your study. You might not have adequate evidence to support your argument if you talk about very recent issues or discoveries. Therefore, make sure you have just the right amount of knowledge and scholarly references to produce a solid biology research paper.


An outline for a biology research paper is essentially a road map for your future work. All of the primary points that you attempt to communicate in each body paragraph must be included in your outline. Consequently, you want to start by outlining your thesis. Then move on to the body of the essay and briefly summarize each paragraph. Each of them ought to contain the main notion and substantiating arguments. Finish with a summary of all the main points and how they relate to the thesis statement.

Look for a biology research paper sample online whenever you get stuck on your plan. They will all have the same format. You’ll have a strong understanding of the optimum format for a biology paper after reading around a dozen of these samples.

Methods and Results in the Body

Your work’s primary body should be composed of components like a technique, a result, and an analysis. This is the main body of your writing, in my opinion. For your thesis statement, you must select the approach that is most pertinent to the situation. These approaches in biology are:

  • historical technique; 
  • bibliographical method; 
  • experiment; 
  • observation; 
  • surveys.

You must proceed to the outcomes once you have finished conducting your experiments or compiling your scientific proof. List the conclusions you’ve reached. Make sure they are pertinent to your work’s goal.

Discussion and Verdict

The discussion and conclusion should come after the main body of your paper is finished. Here, you must succinctly summarize the evidence and conclusions you have drawn. Compare the outcomes to the goals you stated in the introduction. Indicate whether the results support the point that your thesis sought to make. Describe any additional research that is required, if any.


Last but not least, remember to revise and proofread your work. If you are not prepared to make your biology paper stand out in the end, there is no point in learning how to write one. You can step back and evaluate your work as a reader via proofreading. Check to see if you have any weak points. Ensure that your transitions are seamless and simple to understand. Verify your work for typos and grammatical faults.

Even though doing all that work may take some time, your paper will appear fantastic in the end. Impressions are important. Even if you put all the materials together and conduct a successful study, how you present it will affect how people will react to it.

Questions To Study For A Brain Anatomy Quiz In AP Biology

Questions To Study For A Brain Anatomy Quiz In AP Biology

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Taking AP Biology? Have a brain anatomy quiz coming soon? We’ve got 17 questions to help you study for it, plus some clever tricks and tips for studying smarter, not harder!

Parts Of The Brain

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One of the first things you should have to ace a brain anatomy quiz is a thorough grasp of the parts of the brain and each part’s function. Here are some of the questions you might expect:

1. Where Is The Cerebellum Located And What Does It Do?

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The cerebellum is the part of the brain situated at the back of the head. It receives sensory information and regulates your motor movements. The cerebellum also controls balance and coordination, helping you to enjoy smooth movements.

2. Which Part Of The Brain Processes Visual Information?

The occipital lobe lies underneath the occipital bone. It is part of the forebrain (you have two, technically; one at the back of each cortex) and is responsible for processing visual information. Here’s a helpful memory device: the “o” in occipital can remind you of the “o” in optometrist or ophthalmologist.

3. If A Person’s Frontal Lobe Is Injured, What Functions Might He Or She Lose?

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The frontal lobe can be found in the front of the brain, in each cerebral hemisphere. A deep groove called the central sulcus separates it from the parietal lobe, and another groove called the lateral sulcus separates it from the temporal lobe. A part of the frontal lobe known as the precentral gyrus contains the primary motor cortex, which controls specific body parts’ voluntary movements.

The frontal lobe is responsible for reasoning, higher order thinking, and creativity, so if somebody’s frontal lobe is damaged, he or she could have difficulty making decisions and reasoning.

4. What Are The Gyrus And Sulcus And How Do They Help The Brain?

Gyrus are the ridges on the brain and sulcus are the grooves (also seen as furrows or depressions). Together, their up and down “motion” are responsible for the folded, “spaghetti” appearance of the brain.

They are, in fact, an extremely clever way of making the most of very limited space. The brain is limited to the area inside your cranium, but the folding of the brain tissue allows a much greater surface area for cortical tissue, allowing additional cognitive function even in a relatively small space.

The human brain begins as a smooth surface, but as the embryo develops, the brain begins to form the deep indentations and ridges we see in the adult brain.

5. What Part Of The Brain Controls The Primitive Parts Of Our Body?

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Pons is the Latin word for bridge, and that’s exactly what the pons appears to do in the brain, as its physically connected to the brainstem. Like any good bridge, the pons contains neural pathways to move signals to the medulla, cerebellum, and thalamus.

Many of the nuclei contained inside the pons are responsible for relaying signals, as we’ve already described, but other nuclei play roles in primitive functions that we don’t normally consider being within our control, such as respiration, sleep, bladder control, and others.

6. What Is The Corpus Callosum?

The corpus callosum sits underneath the cerebral cortex. It’s about 10cm long and is a thick, tough bundle of fibers that connects the cerebral hemispheres (right and left), enabling them to communicate with each other.

It has over 200 million axonal projections, making it the largest white matter structure.

7. Which Part Of The Brain Is The Newest From An Evolutionary Perspective?

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The cerebrum is the part of the brain that is outermost. In it, the brain can store memories, call upon senses, and establish self-awareness. High order functioning can also take place here and its known for being larger in musicians and left-handed individuals. It is also considered to be the most recent brain development.

8. How Many Lobes Is The Brain Comprised Of, And What Are Their Names And Functions?

Inside the brain is found the occipital lobe (see question #2), the frontal lobe (see question #3), the parietal lobe, and the temporal lobe. The parietal lobe sits behind the frontal lobe and above the temporal lobe. It is where the body becomes self-aware and plays an important role in language processing.

The temporal lobe plays a role in the processing of sensory input, helping the brain to translate these inputs into meaning. If, for example, you smell apple pie and think of your grandmother, you have your temporal lobe to thank!

9. Which Part Of Your Brain Acts Like A Supercomputer?

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The thalamus is the small organ at the very center of your brain that acts as a supercomputer or switchboard, relaying signals throughout the brain. It is one of the most important parts of the brain and regulates motor signals, sleep, and consciousness.

Closely related to the thalamus is the hypothalamus, which sits just underneath the thalamus and regulates the pituitary gland and homeostasis.

10. Which Part Of The Brain Helps You Sneeze?

The medulla oblongata (medulla is Latin for “middle”), and the medulla oblongata is located on the brainstem close to the cerebellum. It is responsible for involuntary or autonomic processes, which include vomiting and sneezing. It also helps with breathing, cardiac functions such as heart rate, and blood pressure.

 The Central Nervous System

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The central nervous system is another important subject likely to show up on a brain anatomy quiz. The questions below will help you better prepare.

11. What Is The Central Nervous System (CNS) Comprised Of?

The brain and the spinal cord make up the CNS, which is protected by the skull and the spine’s vertebral canal. It is the command center of the entire body, regulating all activity and processing all sensory inputs.

 12. What Role Does The Midbrain Play In The CNS?

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The midbrain controls visual reflexes (including automatic eye movements, such as blinking and focusing). It also contains nuclei that link parts of the body’s motor system, including both cerebral hemispheres.

13. What Is A Neurotransmitter?

A neurotransmitter is a chemical that a nerve fiber releases when a nerve impulse arrives. It diffuses across the junction or synapse so that the impulse may pass to the next nerve fiber, muscle fiber, or other structure. Both neurotransmitters and inhibitory neurotransmitters are found in the brain.

14. What Is The Difference Between Dopamine And Serotonin?

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Dopamine and serotonin are both powerful neurotransmitters. Serotonin impacts your sleep, arousal, hunger, and mood, while dopamine impacts your brain’s pleasure and reward system, your learning and attention, and movement.

15. What Is Glutamate And Why Is It Important?

Glutamate is the most abundant neurotransmitter found in the CNS; in fact, it accounts for more than 90% off all the synaptic connections in your brain! Some parts of the brain, including granule cells found in the cerebellum, rely on glutamate almost exclusively. Glutamate also plays a vital role in memory and learning.

16. Can You Name The Most Common Inhibitory Neurotransmitter In The Brain?

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GABA (gamma-Aminobutyric acid) is the most common inhibitory neurotransmitter found in the brain. It is considered inhibitory because it helps to calm or reduce neuron excitability. This means it plays an important role in calming anxiety. It also is responsible for the regulation of muscle tone.

17. What Is The Neurotransmitter That Triggers Our Fight Or Flight Response?

The fight or flight response is also called the acute stress response or hyperarousal; it is a physiological reaction that occurs when the brain perceives an imminent threat. Epinephrine (also known as adrenaline) is the neurotransmitter most responsible for this response. It can signal an increase in blood flow to muscles and greater blood flow through the heart, among other things (this is why your heart starts to beat quickly when you’re afraid).

The Quick Guide To Studying Smarter

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If you’re reading this article, you’re already well on your way to preparing for your brain anatomy quiz, but here are a few more tips to help you get the most out of your time studying:

Get Lots of Rest

Sleeping instead of studying sounds counterintuitive, but without sleep, your brain will have a hard time committing what you’ve learned to memory. In fact, one of the best things you can do to prepare for a test or quiz is to get a good night’s sleep the night before!

Use Memory Devices

We’ve already hinted at a few tricks for helping your brain remember facts (did you notice them in the questions above?), but mnemonic devices and facts set to music help those boring facts stick much better than just rote memorization.

Setting the major parts of the brain to your favorite song, for example, can help pique your brain’s interest and increase emotional arousal, increasing your odds of remembering the information!

Finally, make it real. Drawing the brain, using models of the brain, or reading stories about people who have injured certain parts of the brain are all ways to make abstract concepts seem real–and make you more likely to remember them. Good luck!