Inducing autophagy by rapamycin before, but not after, the formation of plaques and tangles ameliorates cognitive deficits. - Test2 - elhamkhani - TriplyDB

Inducing autophagy by rapamycin before, but not after, the formation of plaques and tangles ameliorates cognitive deficits.

Inducing autophagy by rapamycin before, but not after, the formation of plaques and tangles ameliorates cognitive deficits.

http://www.wikidata.org/entity/Q34043165

about

mTOR is a key modulator of ageing and age-related disease The Function of Autophagy in Neurodegenerative Diseases Dual roles for autophagy: degradation and secretion of Alzheimer's disease Aβ peptide Autophagy and neurodegeneration Mechanisms of age-related macular degeneration The role of tau in neurodegenerative diseases and its potential as a therapeutic target Shedding new light on neurodegenerative diseases through the mammalian target of rapamycin Administration of a selective β2 adrenergic receptor antagonist exacerbates neuropathology and cognitive deficits in a mouse model of Alzheimer's disease Age-dependent neuroinflammation and cognitive decline in a novel Ala152Thr-Tau transgenic mouse model of PSP and AD.Chronic Microdose Lithium Treatment Prevented Memory Loss and Neurohistopathological Changes in a Transgenic Mouse Model of Alzheimer's Disease Potential therapeutic effects of the MTOR inhibitors for preventing ageing and progeria-related disorders ACAT1/SOAT1 as a therapeutic target for Alzheimer's disease Essential role for autophagy in life span extension Pim1 inhibition as a novel therapeutic strategy for Alzheimer's disease Rapalogs and mTOR inhibitors as anti-aging therapeutics Rapamycin attenuates the progression of tau pathology in P301S tau transgenic mice mTOR and neuronal cell cycle reentry: How impaired brain insulin signaling promotes Alzheimer's disease.Nicotinamide forestalls pathology and cognitive decline in Alzheimer mice: evidence for improved neuronal bioenergetics and autophagy procession.mTOR regulates tau phosphorylation and degradation: implications for Alzheimer's disease and other tauopathies.Genetic reduction of mammalian target of rapamycin ameliorates Alzheimer's disease-like cognitive and pathological deficits by restoring hippocampal gene expression signature p62 improves AD-like pathology by increasing autophagy Genetic suppression of β2-adrenergic receptors ameliorates tau pathology in a mouse model of tauopathies.The mammalian target of rapamycin at the crossroad between cognitive aging and Alzheimer's disease.Membrane recruitment of endogenous LRRK2 precedes its potent regulation of autophagy.Longitudinal follow-up of autophagy and inflammation in brain of APPswePS1dE9 transgenic mice The β-secretase-derived C-terminal fragment of βAPP, C99, but not Aβ, is a key contributor to early intraneuronal lesions in triple-transgenic mouse hippocampus.Defective macroautophagic turnover of brain lipids in the TgCRND8 Alzheimer mouse model: prevention by correcting lysosomal proteolytic deficits.Activation of mTOR ameliorates fragile X premutation rCGG repeat-mediated neurodegeneration Induction of autophagy by a novel small molecule improves aβ pathology and ameliorates cognitive deficits Regulation of autophagy by mTOR-dependent and mTOR-independent pathways: autophagy dysfunction in neurodegenerative diseases and therapeutic application of autophagy enhancers.Promoting autophagic clearance: viable therapeutic targets in Alzheimer's disease.Autophagy induction halts axonal degeneration in a mouse model of X-adrenoleukodystrophy.Hippocampal endosomal, lysosomal, and autophagic dysregulation in mild cognitive impairment: correlation with aβ and tau pathology Synthesis, stereochemical analysis, and derivatization of myricanol provide new probes that promote autophagic tau clearance.Acyl-coenzyme A:cholesterol acyltransferase 1 blockage enhances autophagy in the neurons of triple transgenic Alzheimer's disease mouse and reduces human P301L-tau content at the presymptomatic stage.VGF expression by T lymphocytes in patients with Alzheimer's disease Redox regulation of autophagy in healthy brain and neurodegeneration.Stimulation of autophagy reduces neurodegeneration in a mouse model of human tauopathy.Reducing Ribosomal Protein S6 Kinase 1 Expression Improves Spatial Memory and Synaptic Plasticity in a Mouse Model of Alzheimer's Disease.Oxygen-glucose deprivation regulates BACE1 expression through induction of autophagy in Neuro-2a/APP695 cells

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Inducing autophagy by rapamycin before, but not after, the formation of plaques and tangles ameliorates cognitive deficits.

http://www.wikidata.org/entity/Q34043165

description

2011 nî lūn-bûn

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2011 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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name

Inducing autophagy by rapamyci ...... meliorates cognitive deficits.

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Inducing autophagy by rapamyci ...... meliorates cognitive deficits.

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Inducing autophagy by rapamyci ...... meliorates cognitive deficits.

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type

label

Inducing autophagy by rapamyci ...... meliorates cognitive deficits.

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Inducing autophagy by rapamyci ...... meliorates cognitive deficits.

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Inducing autophagy by rapamyci ...... meliorates cognitive deficits.

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prefLabel

Inducing autophagy by rapamyci ...... meliorates cognitive deficits.

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Inducing autophagy by rapamyci ...... meliorates cognitive deficits.

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Inducing autophagy by rapamyci ...... meliorates cognitive deficits.

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P2860

TNF signaling inhibition in the CNS: implications for normal brain function and neurodegenerative disease

Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease

Abeta42-induced neurodegeneration via an age-dependent autophagic-lysosomal injury in Drosophila

Alzheimer's Disease

The pre-autophagosomal structure organized by concerted functions of APG genes is essential for autophagosome formation

Extension of chronological life span in yeast by decreased TOR pathway signaling

Naturally secreted amyloid-beta increases mammalian target of rapamycin (mTOR) activity via a PRAS40-mediated mechanism

LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing

Molecular interplay between mammalian target of rapamycin (mTOR), amyloid-beta, and Tau: effects on cognitive impairments.

Methylene blue reduces aβ levels and rescues early cognitive deficit by increasing proteasome activity

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