Synaptic Oligomers and Glial Cells in Alzheimer Disease

Alzheimer disease (AD) presents an intricate puzzle for researchers and clinicians, with synaptic and neuronal degeneration at the core of its associated cognitive decline. Despite the prominence of the amyloid- β (Aβ) cascade in the AD narrative, attempts to curb disease advancement by eliminating amyloid plaques have yielded limited clinical success. Neurofibrillary tangles, the other hallmark of AD neuropathology, correlate more closely with the loss of synapses and neurons than does Aβ. This evidence highlights the significance of tau alterations associated with the development of AD although the precise mechanisms through which tau abnormalities may lead to neurodegeneration remain poorly comprehended. Recent evidence also underscores neuroinflammation and glia abnormalities as early occurrenc es in AD pathogenesis, thus suggesting an active role of glial cells associated with AD progression. A pioneering article in this issue of JAMA Neurology puts a spotlight on the potential significance of tau oligomers and glial cells in early synaptic loss in AD.

Source: JAMA Neurology - October 9, 2023 Category: Neurology Source Type: research