منابع مشابه
Endophilin2 Interacts with GluA1 to Mediate AMPA Receptor Endocytosis Induced by Oligomeric Amyloid-β
Amyloid-β (Aβ) plays an important role in Alzheimer's disease (AD), as oligomeric Aβ induces loss of postsynaptic AMPA receptors (AMPARs) leading to cognitive deficits. The loss of postsynaptic AMPARs is mediated through the clathrin-dependent endocytosis pathway, in which endophilin2 is one of the important regulatory proteins. Endophilin2, which is enriched in both the pre- and postsynaptic m...
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Amyloid (A ) is thought to play an important role in the pathogenesis of Alzheimer’s disease. A may exert its neurotoxic effects via multiple mechanisms and in particular through degradation of excitatory synaptic transmission associated with impaired synaptic plasticity. In contrast, much less is known about A effects at inhibitory synapses. This study investigates the impact of acute A 1-42 a...
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T he amyloid hypothesis of Alzheimer’s disease (AD) posits that extracellular plaques comprised of the β-amyloid (Aβ) peptide are a root cause of neuronal loss in AD (1). To date, three therapeutic strategies targeting Aβ have been used: (i) inhibiting the production of Aβ, (ii) inhibiting the oligomerization of Aβ, and (iii) promoting the clearance and/or degradation of Aβ. None have led to a ...
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Evidence from neuropathological, genetic, animal model, and biochemical studies has indicated that the accumulation of amyloid-beta (Aβ) is associated with, and probably induces, profound neuronal changes in brain regions critical for memory and cognition in the development of Alzheimer's disease (AD). There is considerable evidence that synapses are particularly vulnerable to AD, establishing ...
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Aggregation of amyloid-beta (Abeta) peptide into soluble and insoluble forms within the brain extracellular space is central to the pathogenesis of Alzheimer's disease. Full-length amyloid precursor protein (APP) is endocytosed from the cell surface into endosomes where it is cleaved to produce Abeta. Abeta is subsequently released into the brain interstitial fluid (ISF). We hypothesized that s...
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ژورنال
عنوان ژورنال: Nature Reviews Neuroscience
سال: 2005
ISSN: 1471-003X,1471-0048
DOI: 10.1038/nrn1754