Alzheimer’s disease is characterized by accumulation of amyloid and neurofibrillary tangles, and this pathology can be detected using neuroimaging or fluid biomarkers prior to the development of dementia. The Alzheimer’s disease process also involves neurodegeneration which eventually leads to cognitive decline and dementia, however typical approaches for measuring neurodegeneration (such as T1-weighted imaging), may not be sensitive to neurodegeneration in the asymptomatic disease stage.
In Alzheimer’s disease (AD), neurodegenerative processes are ongoing for years prior to the time that cortical atrophy can be reliably detected using conventional neuroimaging techniques. Recent advances in diffusion-weighted imaging have provided new techniques to study neural microstructure, which may provide additional information regarding neurodegeneration.
Trimethylamine N-oxide (TMAO), a small molecule produced by the metaorganismal metabolism of dietary choline, has been implicated in human disease pathogenesis, including known risk factors for Alzheimer’s disease (AD), such as metabolic, cardiovascular, and cerebrovascular disease.
To test the hypothesis that cognitively unimpaired individuals with Alzheimer disease (AD) neuropathology differ from individuals with AD dementia on biomarkers of neurodegeneration, synaptic dysfunction, and glial activation.
Myelin and myelin-producing oligodendrocytes appear to be affected in Alzheimer’s disease (AD), but this is understudied in humans, particularly in the early stages of disease development.
Title: Age-dependent differences in brain tissue microstructure assessed with neurite orientation dispersion and density imaging Legend: Healthy brain aging involves substantial changes to the structures that “wire up” the brain, including myelinated axons and dendritic …