The synaptic pathology of cognitive life 
.

The synaptic pathology of cognitive life
. Dialogues Clin Neurosci. 2019 Sep;21(3):271-279 Authors: Honer WG, Ramos-Miguel A, Alamri J, Sawada K, Barr AM, Schneider JA, Bennett DA Abstract Prospective, community-based studies allow evaluation of associations between cognitive functioning and synaptic measures, controlled for age-related pathologies. Findings from >400 community-based participants are reviewed. Levels of two presynaptic proteins, complexin-I (inhibitory terminals), and complexin-II (excitatory terminals) contributed to cognitive variation from normal to dementia. Adding the amount of protein-protein interaction between two others, synaptosome-associated protein-25 and syntaxin, explained 6% of overall variance. The presynaptic protein Munc18-1 long variant was localized to inhibitory terminals, and like complexin-I, was positively associated with cognition. Associations depended on Braak stage, with the level of complexin-I contributing nearly 15% to cognitive variation in stages 0-II, while complexin-II contributed 7% in stages V-VI. Non-denaturing gels identified multiple soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein-protein (SNARE) complexes in frontal and in temporal lobes, making specific contributions to cognitive functions. Multiple mechanisms of presynaptic plasticity contribute to cognitive function during aging.
. PMID: 31749651 [PubMed - in process]
Source: Dialogues in Clinical Neuroscience - Category: Neuroscience Tags: Dialogues Clin Neurosci Source Type: research