Altered expression of synaptic proteins occurs early during progression of Alzheimer’s disease
By E. Masliah, M. Mallory, M. Alford, R. Deteresa, L. Hansen, D. McKeel, J. Morris. Neurology, 2001
713 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/3537794bbd1c60569fc0184ff3c069da496585ee
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Citations in the corpus
- Impaired Balance of Mitochondria Fission and Fusion in Alzheimer Disease (2009, background): “A is a homeostatic regulator of synaptic strength (Kamenetz et al., 2003), suggesting that perturbations in soluble A levels might be linked to the learning and memory deficits in AD patients (Masliah et al., 2001).”
- Tau mislocalization to dendritic spines mediates synaptic dysfunction independently of neurodegeneration (2010, background): “Understanding the early pathological events preceding synapse loss in neurodegenerative diseases is of critical relevance since synaptic loss correlates more robustly with cognitive deficits in AD than plaque or tangle load (Davies et al., 1987; Terry et al., 1991; Masliah et al., 2001; Selkoe, 2002”
- Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease (2018, background): “It has been reported that synaptic failures occur from an early stage in the AD brain and that the levels of synaptic proteins change (Masliah et al., 2001).”
- Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior. (2008, background): “…with AD contributes to the pathogenesis of the disease and may underlie the synapse loss in hippocampus that occurs early in the disease process and is a key quantitative correlate of degree of cognitive impairment in AD patients (Davies et al. 1987; Masliah et al. 2001; Terry et al. 1991).”
- Classification and basic pathology of Alzheimer disease (2009, background): “Synaptophysin was found to be decreased at early stages of the disease [219], leading to the conclusion that synaptic 18 Acta Neuropathol (2009) 118:5–36”
- The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice. (2008, background): “Abeta deposition is associated with neuropil changes, but not with overt neuronal loss in the human amyloid precursor protein V717F (PDAPP) transgenic mouse.”