ArticleAlzheimer's research & therapy2021
P-tau and neurodegeneration mediate the effect of β-amyloid on cognition in non-demented elders.
Article in Alzheimer's research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.
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Who cites it
8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.
- Association of soluble TREM2 with Alzheimer's disease and mild cognitive impairment: a systematic review and meta-analysis.Frontiers in aging neuroscience · 2024Pooled it
- Regulatory role of the endocannabinoid system on glial cells toward cognitive function in Alzheimer's disease: A systematic review and meta-analysis of animal studies.Frontiers in pharmacology · 2023Pooled it
- Alzheimer's Biomarkers and Visuospatial Cognition in Parkinson's Disease: Modification by α-Synuclein and Mediation of Age Effects.Movement disorders clinical practice · 2026Article
- Sex differences in vulnerability to tau pathology: Impact on cognitive decline.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Association of hemoglobin with plasma neurofilament light and white matter hyperintensities in Alzheimer's disease continuum.Heliyon · 2024Article
- Association of triglyceride glucose-body mass index with Alzheimer's disease pathology, cognition and brain structure in non-demented people.Scientific reports · 2024Article
- Soluble TREM2 in body fluid in Alzheimer's disease and Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- Plasma Biomarkers of Alzheimer's Disease Are Associated with Physical Functioning Outcomes Among Cognitively Normal Adults in the Multiethnic HABS-HD Cohort.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThere 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).
methodsThree hundred seventy normal controls (CN) and 623 MCI patients from the ADNI (Alzheimer's Disease Neuroimaging Initiative) database were recruited in this research. Linear mixed-effects models were used to evaluate the associations of baseline Aβ with cognitive decline and biomarkers of several pathophysiological pathways. Causal mediation analyses with 10,000 bootstrapped iterations were conducted to explore the mediation effects of AD pathologies on cognition.
resultsTau-related pathology, neurodegeneration, neuroinflammation are correlated with the concentration of Aβ, even in CN participants. The results show that age, gender, and APOE ε4 carrier status have a moderating influence on some of these relationships. There is a stronger association of Aβ with biomarkers and cognitive changes in the elderly and females. In CN group, Aβ pathology is directly related to poor cognition and has no mediating effect (p < 0.05). In mild cognitive impairment, tau-related pathology (26.15% of total effect) and neurodegeneration (14.8% to 47.0% of total effect) mediate the impact of Aβ on cognition.
conclusionsIn conclusion, early Aβ accumulation has an independent effect on cognitive decline in CN and a tau, neurodegeneration-dependent effect in the subsequent cognitive decline in MCI patients.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.