The Progression Of Alzheimer’s Disease Immunotherapy

Alzheimer’s disease (AD) is one of a series of neurodegenerativediseases characterized by the conformational change of a normal proteininto a abnormal conformer with a high β-sheet content that renders itagainst to degradation and neurotoxic.In the case of AD the normal solubleamyloid β (sAβ) peptide is converted into oligomeric/fibrillar Aβ. Theoligomeric forms of Aβ are thought to be the most neurotoxic, whilefibrillar Aβ becomes deposited as amyloid plaques and congophilicangiopathy, which both serve as neuropathological markers of the disease.Besides, the aggregation of abnormal tau protein as soluble toxic oligomersand as neurofibrillary tangles is an important part of the diseaes. Manytherapies are under study to prevent progresion of AD and treat AD. Thetesting of these diverse approaches to ameliorate AD pathology has beenmade possible by the existence of numerous transgenic mouse modelswhich each mirror different aspects of AD pathology. Perhaps the mostexciting of these approaches is immunomodulation. Vaccination iscurrently being tried for a range of age associated CNS disorders with great success being reported in many transgenic mouse models.However, there isa discrepancy between these results and current human clinical trials whichhighlights the limitations of current models and also uncertainties in ourunderstanding of the underlying pathogenesis of AD. Existent mousemodel of Alzheimer’s disease doesn’t exactly reflects all character of ADpatients. Because of the underlying etiology of sporadic AD is unknown,the process of creating better Tg models is in continual evolution. This is ancapital goal since it will be important to AD develop therapises which willbe highly significant in humans. In this review, we will provide an updateof Aβ immunotherapy in animal models and in human beings, as well asdiscuss the possible mechanisms underlying Aβ immunotherapy for AD.