ArticleThe Journal of biological chemistry2011
Membrane cholesterol modulates {beta}-amyloid-dependent tau cleavage by inducing changes in the membrane content and localization of N-methyl-D-aspartic acid receptors.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- The formation of small aggregates contributes to the neurotoxic effects of tauNeurochemistry international · 2022Article
- Role of the Lipid Membrane and Membrane Proteins in Tau Pathology.Frontiers in cell and developmental biology · 2021Review
- Melatonin Alters Fluid Phase Coexistence in POPC/DPPC/Cholesterol Membranes.Biophysical journal · 2020Article
- Effects of Cholesterol in Stress-Related Neuronal Death-A Statistical Analysis Perspective.International journal of molecular sciences · 2020Article
- Involvement of calpain in the neuropathogenesis of Alzheimer's disease.Medicinal research reviews · 2019Review
- TauNeuroscience · 2017Article
- Extracellular truncated tau causes early presynaptic dysfunction associated with Alzheimer's disease and other tauopathies.Oncotarget · 2017Article
- Upregulation of calpain activity precedes tau phosphorylation and loss of synaptic proteins in Alzheimer's disease brain.Acta neuropathologica communications · 2016Article
- Calpain cleavage and inactivation of the sodium calcium exchanger-3 occur downstream of Aβ in Alzheimer's disease.Aging cell · 2014Article
- Calpain dysregulation in Alzheimer's disease.ISRN biochemistry · 2012Review
- Calpain-mediated tau cleavage: a mechanism leading to neurodegeneration shared by multiple tauopathies.Molecular medicine (Cambridge, Mass.) · 2011Article
- Implicating calpain in tau-mediated toxicity in vivo.PloS one · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We have previously shown that β-amyloid (Aβ) treatment resulted in an age-dependent calpain activation leading to Tau cleavage into a neurotoxic 17-kDa fragment in a cellular model of Alzheimer disease. This detrimental cellular response was mediated by a developmentally regulated increase in membrane cholesterol levels. In this study, we assessed the molecular mechanisms by which cholesterol modulated Aβ-induced Tau cleavage in cultured hippocampal neurons. Our results indicated that these mechanisms did not involve the regulation of the binding of Aβ aggregates to the plasma membrane. On the other hand, experiments using N-methyl-d-aspartic acid receptor inhibitors suggested that these receptors played an essential role in cholesterol-mediated Aβ-dependent calpain activity and 17-kDa Tau production. Biochemical and immunocytochemical analyses demonstrated that decreasing membrane cholesterol levels in mature neurons resulted in a significant reduction of the NR1 subunit at the membrane as well as an increase in the number of large NR1, NR2A, and NR2B subunit clusters. Moreover, the majority of these larger N-methyl-d-aspartic acid receptor subunit immunoreactive spots was not juxtaposed to presynaptic sites in cholesterol-reduced neurons. These data suggested that changes at the synaptic level underlie the mechanism by which membrane cholesterol modulates developmental changes in the susceptibility of hippocampal neurons to Aβ-induced toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.