Biomarkers predicting Alzheimer's disease in cognitively normal aging

Abstract

The pathophysiologic process of Alzheimer's disease (AD) begins years before the diagnosis of clinical dementia. This concept of preclinical AD has arisen from the observation of AD pathologic findings such as senile plaques and neurofibrillary tangles in the brains of people who at the time of death had normal cognitive function. Recent advances in biomarker studies now provide the ability to detect the pathologic changes of AD, which are antecedent to symptoms of the illness, in cognitively normal individuals. Functional and structural brain alterations that begin with amyloid-β accumulation already show the patterns of abnormality seen in individuals with dementia due to AD. The presence of preclinical AD provides a critical opportunity for potential interventions with disease-modifying therapy. This review focuses on the studies of antecedent biomarkers for preclinical AD.

Keywords: Alzheimer's disease; biomarker; preclinical.

Fig. 1

Hypothetical cascade of pathophysiology and related biomarkers in Alzheimer's disease (AD). APP: amyloid precursor protein, CSF: cerebrospinal fluid, Aβ: amyloid beta, SP: senile plaque, NFT: neurofibrillary tangle, PIB: pittsburg compound B, p-tau: phosphorylated tau, FDG: fluorodeoxyglucose, PET: positron-emission tomography, MRI: magnetic resonance imaging.