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ABSTRACT: Background
The loss of synaptic function is a pivotal mechanism in the development of Alzheimer's Disease (AD). Structural changes and loss of plasticity in the postsynaptic density (PSD) may contribute to the pathogenesis. However, the underlying molecular events triggering synaptic dysfunction remain elusive. We report a quantitative proteomic analysis of the PSD from human postmortem brain tissues of possible and definite AD cases.Methods
The analysis used both discovery and targeted mass spectrometry approaches and was repeated with biological replicates. During the discovery study, we compared several hundred proteins in the PSD-enriched fractions and found that 25 proteins were differentially regulated in AD.Results
Interestingly, the majority of these protein
SUBMITTER: Zhou J
PROVIDER: S-EPMC3714371 | biostudies-literature | 2013 May
REPOSITORIES: biostudies-literature