In people with AD, the presence of amyloid beta is believed to trigger a pathological cascade that may promote the abnormal phosphorylation of tau protein, which leads to the formation of neurofibrillary tangles within neurons.1,2
Together, abnormal accumulation of amyloid beta plaques and neurofibrillary tangles can impair neuronal function and may cause neurodegeneration (atrophy).1,3
According to the cascade hypothesis, amyloid beta accumulation is the earliest marker of Alzheimer's disease pathology, occurring upstream of synaptic dysfunction and tau-mediated neuronal injury.5
This makes biomarker confirmation via amyloid positron emission tomography (PET) scan or cerebrospinal fluid (CSF) test all the more important. The diagnostic value of AD as the cause of MCI provides the clinician an opportunity to take action before greater neuronal damage occurs and more cognition and function are lost.6
Support a diagnosis of AD in the MCI stage with biomarkers.