Perspective reveals the link between basal forebrain volume and amyloid burden, suggesting early signs of Alzheimer's in older adults at genetic risk.
Alzheimer's disease (AD) is a progressive neurodegenerative disease that is typified by cognitive and functional deterioration. Biologically it is driven by the aggregation of misfolded amyloid-β (Aβ) oligomers and the phosphorylation of neurofibrillary tau proteins, both of which have been observed to occur years before the onset of clinical and functional symptoms.1,2 Aβ accumulation, observed prior to tau, has therefore been seen as the initial hallmark of future AD progression. This cascading pattern has shaped the direction of current investigations, by focusing on understanding the initial spread of Aβ in cognitively unimpaired individuals, to examine how best to mitigate future cognitive decline.
No takes yet. Share an insight, caveat, or question.
Alexander C. Conley (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: