β-Amyloid peptides are the major constituents of senile plaques and neurofibrillary tangles that occur in the hippocampus, neocortex, and amygdala of patients with Alzheimer′s disease. Aβ (1-40) whether soluble or insoluble differentiates AD vs high pathology controls. The Arctic mutation E22G causes early onset of Alzheimer′s compared to wild type and promotes protofibril formation and neurotoxicity.
Amyloid β-peptide (Aβ) is directly linked to Alzheimer's disease (AD). In its monomeric form, Aβ aggregates to produce fibrils and a range of oligomers, the latter being the most neurotoxic. Dysregulation of Ca(2+) homeostasis in aging brains and in neurodegenerative
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