Issue Information

Front coverIncreasing NAA synthase (Nat8L) via AAV-mediated overexpression in a model of Alzheimer's Disease compromises mitochondrial energy metabolism. Sequestration of mitochondrial aspartate by NAA is incompatible with pathological energetic crisis, accelerates associated cognitive decline and presents a rationale for the active reduction of NAA in a broad clinical spectrum of neurodegenerative disease.Image contentOverexpression of NAA synthase (Nat8L) in hippocampal Neurons of 5xFAD mice compounds phenotypic energy deficit and accelerates cognitive decline.Read the full article‘Over-expression of N-acetylaspartate synthase exacerbates pathological energetic deficit and accelerates cognitive decline in the 5xFAD mouse ’ by J. S. Francis, Q. Nguyen, V. Markov and P. Leone (J. Neurochem. vol. 168 (2), pp. 69 –82) on doi:10.1111/jnc.16044
Source: Journal of Neurochemistry - Category: Neuroscience Tags: ISSUE INFORMATION Source Type: research