The Working Group recommended that certain AD biomarkers – structural MRI, brain amyloid imaging and cerebrospinal fluid levels of amyloid beta-protein 42 (AB42) and tau – should be used for enrollment and as an outcome in AD clinical trials, along with current clinical assessments, such as neuropsychological testing and the mini-mental state exam (MMSE) and assessment of activities of daily living (ADL). However, the Group also noted that AD biomarkers must undergo validation and reliability studies in non-research settings before their clinical utility in clinical practice can be determined.
Biomarkers for AD can be divided broadly into those that identify the aspects of the molecular pathology of AD and those that reflect the "downstream" consequences of that pathology. The neuropathological hallmarks that define AD are the amyloid plaques and neurofibrillary tangles found in the brains of AD patients upon autopsy. Amyloid plaques develop when the AB 42 protein accumulates in increasingly insoluble forms, and neurofibrillary tangles develop when tau proteins accumulate inside neurons and form insoluble filaments. Both AB 42 and tau can be measured in cerebrospinal fluid.
Certain imaging tests detect more "downstream" events that follow events initiated at the molecular level. For example, structural magnetic resonance imaging (MRI) can help detect neuronal loss and brain shrinkage caused by AD.
The Alliance for Aging Research and a coalition of non-profit organizations it chairs kno
|SOURCE Alliance for Aging Research|
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