The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism. - Wikidata - awgldk - TriplyDB

The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism.

The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism.

http://www.wikidata.org/entity/Q35578655

about

Presenilin-1 regulates the expression of p62 to govern p62-dependent tau degradation Familial Alzheimer disease-linked mutations specifically disrupt Ca2+ leak function of presenilin 1 BRI3 inhibits amyloid precursor protein processing in a mechanistically distinct manner from its homologue dementia gene BRI2 Apolipoprotein E and its receptors in Alzheimer's disease: pathways, pathogenesis and therapy MicroRNA: Implications for Alzheimer Disease and other Human CNS Disorders Presenilins are essential for regulating neurotransmitter release Amyloid precursor protein regulates brain apolipoprotein E and cholesterol metabolism through lipoprotein receptor LRP1 Synapses and Alzheimer's disease Inactivation of presenilins causes pre-synaptic impairment prior to post-synaptic dysfunction The amyloid hypothesis of Alzheimer's disease at 25 years Cellular mechanisms of γ-secretase substrate selection, processing and toxicity New pharmacological strategies for treatment of Alzheimer's disease: focus on disease modifying drugs The genetics and neuropathology of Alzheimer's disease Protease regulation: the Yin and Yang of neural development and disease Toward the structure of presenilin/γ-secretase and presenilin homologs Inconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer's disease Cortical odor processing in health and disease Lysosome and calcium dysregulation in Alzheimer's disease: partners in crime 3D culture models of Alzheimer's disease: a road map to a "cure-in-a-dish"Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1 Phenylbutyric acid rescues endoplasmic reticulum stress-induced suppression of APP proteolysis and prevents apoptosis in neuronal cells Transgenic expression of the amyloid-beta precursor protein-intracellular domain does not induce Alzheimer's Disease-like traits in vivo Molecular profiling reveals diversity of stress signal transduction cascades in highly penetrant Alzheimer's disease human skin fibroblasts Lysosomal proteolysis and autophagy require presenilin 1 and are disrupted by Alzheimer-related PS1 mutations Partial loss of presenilin impairs age-dependent neuronal survival in the cerebral cortex Generation and initial characterization of FDD knock in mice Roles of 3-nitrotyrosine- and 4-hydroxynonenal-modified brain proteins in the progression and pathogenesis of Alzheimer's disease.Brain gene expression of a sporadic (icv-STZ Mouse) and a familial mouse model (3xTg-AD mouse) of Alzheimer's disease.A novel function for the presenilin family member spe-4: inhibition of spermatid activation in Caenorhabditis elegans Apolipoprotein E-mimetics inhibit neurodegeneration and restore cognitive functions in a transgenic Drosophila model of Alzheimer's disease Characterization of age-dependent and progressive cortical neuronal degeneration in presenilin conditional mutant mice.Chemical and morphological alterations of spines within the hippocampus and entorhinal cortex precede the onset of Alzheimer's disease pathology in double knock-in mice Presenilins and the gamma-secretase: still a complex problem.Presenilin controls CBP levels in the adult Drosophila central nervous system.Presenilin 2 is the predominant γ-secretase in microglia and modulates cytokine release Genetics of Alzheimer disease in the pre- and post-GWAS era Presenilin/γ-secretase regulates neurexin processing at synapses Presenilin conditional double knockout mice exhibit decreases in drebrin a at hippocampal CA1 synapses Presenilin/gamma-Secretase and Inflammation.A presenilin-1 mutation identified in familial Alzheimer disease with cotton wool plaques causes a nearly complete loss of gamma-secretase activity

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P2860

The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism.

http://www.wikidata.org/entity/Q35578655

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Jie Shen

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P2860

Presenilin 1 is linked with gamma-secretase activity in the detergent solubilized state

A presenilin-1/gamma-secretase cleavage releases the E-cadherin intracellular domain and regulates disassembly of adherens junctions.

Presenilins form ER Ca2+ leak channels, a function disrupted by familial Alzheimer's disease-linked mutations

The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics

Presenilin 1 facilitates the constitutive turnover of beta-catenin: differential activity of Alzheimer's disease-linked PS1 mutants in the beta-catenin-signaling pathway

A transcriptionally [correction of transcriptively] active complex of APP with Fe65 and histone acetyltransferase Tip60

Skeletal and CNS defects in Presenilin-1-deficient mice

Familial Alzheimer's disease mutations inhibit gamma-secretase-mediated liberation of beta-amyloid precursor protein carboxy-terminal fragment

Presenilin clinical mutations can affect gamma-secretase activity by different mechanisms

Regulation of NMDA receptor trafficking by amyloid-beta

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