Pathophysiology and Disease Mechanisms

Alzheimer’s disease is a progressive dementia with loss of neurons and the presence of two main microscopic neuropathological hallmarks: extracellular amyloid plaques and intracellular neurofibrillary tangles. Early onset AD, a rare familial form, is caused due to mutation of one out of three genes: (amyloid precursor protein), (presenilin 2) or (presenilin 1).  Sporadic form occurs usually after age of 65 and accounts for most cases; it most likely results from a combination of genetic and influence of environment. Confirmed risk factors for sporadic AD are age and the presence of the E4 allele of (Apo lipoprotein E). Amyloid plaques comprise mainly of the neurotoxic peptide amyloid (Aβ, Abeta), cleaved sequentially from a larger precursor protein (APP) by two enzymes: β-secretase (also called BACE1) and γ-secretase (comprising four proteins, presenilin is one of them). If APP is first cleaved by the enzyme α-secretase rather than β-secretase then Aβ is not formed. Neurofibrillary tangles comprise mainly of the protein tau which binds with microtubules, which facilitating the neuronal transport system. Tau uncoupling from microtubules and aggregation into tangles inhibits transport and results in disassembly of microtubule. Phosphorylation of tau might have an important role in this. Selective vulnerability of neuronal systems such as the cholinergic, serotonergic, and noradrenergic and glutamatergic systems form the basis of current rational pharmacological treatment.

This session includes Aging, Prions and Alzheimer’s disease, Cellular signaling and cell to cell transmission, Oxidative damage and mitochondrial dysfunction, Autoimmunity in Alzheimer’s, Blood-brain barrier and transport, Neurogenesis and stem cells and Cell death.

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