Blood Biomarkers of Alzheimer's Disease are Early Predictors of Dementia Risk
Alzheimer's disease is a slow condition, in which brain biochemistry changes for the worse over a span of many years prior to evident symptoms. Considerable progress has been made in the matter of finding markers that reflect those changes, a way to determine future risk of dementia. At some point these markers will be actionable in ways other than being a spur to change lifestyle for the better, doing so in the hopes of slowing down the progression of neurodegenerative processes. For now, however, at least there are some signposts on the way to cognitive decline.
Alzheimer's disease (AD) and related dementias feature a prolonged preclinical stage spanning decades, with the transition from midlife to late life marking the critical period for the onset and accumulation of pathological brain changes. Plasma biomarkers have shown great promise in becoming a cost-effective and noninvasive screening tool for AD pathology and neurodegeneration in symptomatic persons, but their presymptomatic trajectories are not well understood.
Using the well-established community-based Atherosclerosis Risk in Communities study, we characterized temporal changes in plasma biomarkers, identified factors associated with changes in plasma biomarkers over time, and evaluated the prospective associations of plasma biomarkers with late-life all-cause dementia. Analyses were conducted overall and stratified by demographics (sex, race), apolipoprotein E epsilon 4 (APOE ε4) allele status, and cognitive diagnosis.
In this retrospective analysis of prospectively collected plasma biomarkers from 1,525 adults from the Atherosclerosis Risk in Communities study, only Alzheimer disease (AD)-specific (Aβ42:Aβ40 ratio and p-Tau181) biomarkers in midlife demonstrated significant long-term associations with late-life dementia. In late life, each of the biomarkers and their change from midlife were significantly associated with incident all-cause dementia.
Elevated homocysteine is greatly associated with cognitive decline and can be corrected with glutamate and methionine reduction and adding betaine and the b vitamins.