P-tau and neurodegeneration mediate the effect of β-amyloid on cognition in non-demented elders.

ABSTRACT:

Background

There are many pathological changes in the brains of Alzheimer's disease (AD) patients. For many years, the mainstream view on the pathogenesis of AD believes that β-amyloid (Aβ) usually acts independently in addition to triggering functions. However, the evidence now accumulating indicates another case that these pathological types have synergies. The objective of this study was to investigate whether effects of Aβ pathology on cognition were mediated by AD pathologies, including tau-related pathology (p-tau), neurodegeneration (t-tau, MRI measurements), axonal injury (NFL), synaptic dysfunction (neurogranin), and neuroinflammation (sTREM2, YKL-40).

Methods

Three hundred seventy normal controls (CN) and 623 MCI patients from the ADNI (Alzheimer's Disease Neuroima

SUBMITTER: Ma LZ 

PROVIDER: S-EPMC8675473 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature