Diagnostic and Prognostic Utility of the Synaptic Marker Neurogranin in Alzheimer Disease

Abstract

The aggregation and deposition of amyloid-β (Aβ) and tau, the 2 key proteins involved in Alzheimer disease (AD) pathogenesis, are estimated to begin years before the onset of cognitive impairment.^1,2 However, the first signs of cognitive impairment only appear after significant neuronal and synaptic loss has occurred in vulnerable brain regions.³ Neuronal and synaptic loss reflects the cumulative outcome of different pathologic substrates in AD and, therefore, may provide the best surrogate for clinical and radiologic disease progression.^2,4-7