Capetillo-Zarate E, Gracia L, Tampellini D, Gouras GK. (2012) Intraneuronal Aβ accumulation, amyloid plaques, and synapse pathology in Alzheimer's disease. Neurodegener Dis Jan 21 [Epub ahead of print]Capetillo-Zarate E,Gracia L,Tampellini D, et al.Intraneuronal Abeta Accumulation, ...
The aberrant accumulation of aggregated β-amyloid peptides (Aβ) as plaques is a hallmark of Alzheimer’s disease (AD) neuropathology and reduction of Aβ has become a leading direction of emerging experimental therapies for the disease. The mechanism(s) whereby Aβ is involved in the pathophy...
K., Gambetti, P.: The pathology of the synapse in Alzheimer's disease. In: G. E. W. Wolstenholme and M. O'Connor (eds.): Alzheimer's Disease, CIBA Symposium, pp. 169–183. London: Churchill 1970Gonatas, N. and Gambetti, P. 1970. The pathology of the synapse in Alzheimer's ...
Collapsin Response Mediator Protein-2 (CRMP2) is a Plausible Etiological Factor and Potential Therapeutic Target in Alzheimer's Disease: Comparison and Con... Alzheimer's disease (AD) has long been viewed as a pathology that must be caused either by aberrant amyloid-β protein precursor (AβPP...
the pathology of Alzheimer disease (AD) as it catalyzes the final step in the process- ing of the amyloid precursor protein (APP) leading to the formation of the neurotoxic amyloid β-peptide (Aβ), which is the major constituent of the amyloid plaques in the brains of AD patients [1]....
Alzheimer’s disease (AD) is a neurodegenerative disorder with devastating symptoms, including memory impairments and cognitive deficits. Hallmarks of AD pathology are amyloid-beta (Aβ) deposition forming neuritic plaques and neurofibrillary tangles (NF
Calpain hyperactivation is implicated in late-stages of neurodegenerative diseases including Alzheimer’s disease (AD). However, calpains are also critical for synaptic function and plasticity, and hence memory formation and learning. Since synaptic defi
To further test the hypothesis that this fundamental signaling pathway is a primary target of synapse degeneration in Alzheimer’s disease, the Zou lab used 5XFAD mice, a well-known mouse model of amyloid beta pathology. This transgenic mouse carries five human mutations that cause Alzhe...
Objective Currently no effective disease-modifying agents exist for the treatment of Alzheimer disease (AD). The Fyn tyrosine kinase is implicated in AD pathology triggered by amyloid- oligomers (Ao) and propagated by Tau. Thus, Fyn inhi... AC Kaufman,SV Salazar,LT Haas,... - 《Annals of...
However, with regard to synapse formation, Gsk-3β has been implicated in the transport of amyloid precursor protein (APP) in axons, and in the wnt signaling pathway. Although the role of APP outside of the pathway to Alzheimer’s disease remains elusive, interactome studies suggest that APP...