Synaptic degeneration and neurogranin in the pathophysiology of Alzheimer's disease. (2nd January 2017)

• Record Type: Journal Article
• Authors: Lista, Simone; Hampel, Harald
• Is Part Of: Expert review of neurotherapeutics. Volume 17:Number 1(2017)
• Page Start: 47
• Page End: 57
• Publication Date: 2017-01-02
• Subjects: Alzheimer's disease -- synaptic dysfunction -- amyloid beta -- tau protein -- neurogranin -- biomarker -- cerebrospinal fluid -- pathophysiology -- early diagnosis -- precision medicine; Neuropharmacology -- Periodicals; 615.7805
• DOI: 10.1080/14737175.2016.1204234
• Languages: English
• ISSNs: 1473-7175

Abstract

ABSTRACT: Introduction : Synaptic dysfunction and degeneration are early fundamental pathophysiological characteristics of Alzheimer's disease (AD). In addition, synaptic depletion closely correlates with clinical disease severity. Biomarkers that may track synaptic dysfunction in AD are eagerly awaited. Areas covered : Here, we reviewed the significance of the post-synaptic protein neurogranin – particularly enriched in dendritic spines – as a biomarker of early synaptic dysfunction in AD. We also examined its role as a marker to predict disease progression. Expert commentary : Current evidence indicates that neurogranin may serve as a mechanism-of-action biomarker aiding the in vivo investigation of AD-related pathophysiological pathways. Its use may support the development of targeted therapeutic interventions tailored to the individual patient, i.e. 'molecularly' targeted therapies, according to the evolving precision medicine paradigm.