Alzheimer's disease is a progressive dementia with neuron loss and two major neuropathological microscopic characteristics: extracellular amyloid plaques and intracellular neurofibrillary tangles. Early onset of AD, a rare family form, is caused by one of three genes mutating: (amyloid precursor protein), (presenilin 2) or (presenilin 1). Sporadic form usually occurs after 65 years of age and is accountable in most cases; it most likely results from a combination of genetic and influence of environment. The age and presence of the E4 alllele (Apo lipoprotein E) are confirmed risk factors for sporadic AD. Amyloid plaques consist mainly of neurotoxic peptide amyloid (A?, Abeta), sequentially cleaved by two enzymes from a larger precursor protein (APP): ?-secretase (also referred to as BACE1) and ?-secretase (composed of four proteins, one of which is preseniline). If APP is cleaved by the ?-secretase enzyme instead of ?-secretase, A? is not formed. Neurofibrillary tangles mainly consist of the protein tau that binds to microtubules and facilitates the neuronal transport system. Tau disassembly from microtubules and aggregation into tangles prevents transport and leads to microtubule disassembly. Tau phosphorylation could play an important role in this. The current rational pharmacological treatment is based on the selective vulnerability of neuronal systems, such as cholinergic, serotonergic and noradrenergic and glutamatergic systems.
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.