Recent biomarker studies suggest that the pathological changes of Alzheimer disease (AD) start with Aβ deposition as early as 20 to 30 years prior to symptom onset,1 a window of time that holds promise for therapeutic intervention to reverse or slow down the disease. Aβ deposition is believed to be followed by tangle pathology and neurodegeneration (as reflected by concentrations of tau protein in cerebrospinal fluid [CSF]) some 10 to 20 years later and closer to clinical disease onset, which resonates well with the Aβ cascade hypothesis in which Aβ is regarded as the trigger and potentially also the driver in the disease process.
Zetterberg H, Blennow K. Neurogranin Levels in Cerebrospinal FluidA New Addition to the Alzheimer Disease Diagnostic Toolbox. JAMA Neurol. 2015;72(11):1237-1238. doi:10.1001/jamaneurol.2015.2075