Dun‐Sheng Yang
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View article: Pathobiology of the autophagy-lysosomal pathway in the Huntington’s disease brain
Pathobiology of the autophagy-lysosomal pathway in the Huntington’s disease brain Open
Background Accumulated levels of mutant huntingtin protein (mHTT) and its fragments are considered contributors to the pathogenesis of Huntington’s disease (HD). Stimulating autophagy may enhance clearance of mHTT and its aggregates which …
View article: mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance
mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance Open
Huntington’s disease (HD) is caused by the expansion of the polyglutamine stretch in huntingtin protein (HTT) resulting in hallmark aggresomes/inclusion bodies (IBs) composed of mutant huntingtin protein (mHTT) and its fragments. Stimulati…
View article: Author response: mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance
Author response: mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance Open
View article: Author response: mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance
Author response: mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance Open
View article: mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance
mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance Open
Huntington’s disease (HD) is caused by expansion of the polyglutamine stretch in huntingtin protein (HTT) resulting in hallmark aggresomes/inclusion bodies (IBs) composed of mutant huntingtin protein (mHTT) and its fragments. Stimulating a…
View article: mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance
mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance Open
Huntington’s disease (HD) is caused by the expansion of the polyglutamine stretch in huntingtin protein (HTT) resulting in hallmark aggresomes/inclusion bodies (IBs) composed of mutant huntingtin protein (mHTT) and its fragments. Stimulati…
View article: mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance
mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance Open
Huntington’s disease (HD) is caused by expansion of the polyglutamine stretch in huntingtin protein (HTT) resulting in hallmark aggresomes/inclusion bodies (IBs) composed of mutant huntingtin protein (mHTT) and its fragments. Stimulating a…
View article: Autophagy-lysosomal dysfunction, intraneuronal amyloidosis, and selective neuron death yield senile plaques in preclinical late-onset Alzheimer’s Disease
Autophagy-lysosomal dysfunction, intraneuronal amyloidosis, and selective neuron death yield senile plaques in preclinical late-onset Alzheimer’s Disease Open
The autophagy-lysosomal pathway (ALP) is dysfunctional in Alzheimer’s Disease (AD) although pathogenic consequences remain unclear. Here, we identify exceptionally early ALP dysfunction in neocortical neurons of late-onset sporadic AD (LOA…
View article: mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance
mTOR inhibition in Q175 Huntington’s disease model mice facilitates neuronal autophagy and mutant huntingtin clearance Open
Huntington’s disease (HD) is caused by expansion of the polyglutamine stretch in huntingtin protein (HTT) resulting in hallmark aggresomes/inclusion bodies (IBs) composed of mutant huntingtin protein (mHTT) and its fragments. Stimulating a…
View article: Pathobiology of the autophagy-lysosomal pathway in the Huntington’s disease brain
Pathobiology of the autophagy-lysosomal pathway in the Huntington’s disease brain Open
Accumulated levels of mutant huntingtin protein (mHTT) and its fragments are considered contributors to the pathogenesis of Huntington’s disease (HD). Although lowering mHTT by stimulating autophagy has been considered a possible therapeut…
View article: Autophagy is a novel pathway for neurofilament protein degradation <i>in vivo</i>
Autophagy is a novel pathway for neurofilament protein degradation <i>in vivo</i> Open
How macroautophagy/autophagy influences neurofilament (NF) proteins in neurons, a frequent target in neurodegenerative diseases and injury, is not known. NFs in axons have exceptionally long half-lives in vivo enabling formation of …
View article: Preclinical and randomized clinical evaluation of the p38α kinase inhibitor neflamapimod for basal forebrain cholinergic degeneration
Preclinical and randomized clinical evaluation of the p38α kinase inhibitor neflamapimod for basal forebrain cholinergic degeneration Open
View article: Faulty autolysosome acidification in Alzheimer’s disease mouse models induces autophagic build-up of Aβ in neurons, yielding senile plaques
Faulty autolysosome acidification in Alzheimer’s disease mouse models induces autophagic build-up of Aβ in neurons, yielding senile plaques Open
Autophagy is markedly impaired in Alzheimer’s disease (AD). Here we reveal unique autophagy dysregulation within neurons in five AD mouse models in vivo and identify its basis using a neuron-specific transgenic mRFP-eGFP-LC3 probe of autop…
View article: Preclinical and Clinical Studies of p38α MAP kinase inhibition to Treat Basal Forebrain Cholinergic Dysfunction and Degeneration
Preclinical and Clinical Studies of p38α MAP kinase inhibition to Treat Basal Forebrain Cholinergic Dysfunction and Degeneration Open
The endosome-associated protein Rab5 is a central player in the molecular mechanisms leading to degeneration of basal forebrain cholinergic neurons (BFCN), a long-standing target for drug development. As p38α kinase is a Rab-5 activator, w…
View article: Post-Golgi carriers, not lysosomes, confer lysosomal properties to pre-degradative organelles in normal and dystrophic axons
Post-Golgi carriers, not lysosomes, confer lysosomal properties to pre-degradative organelles in normal and dystrophic axons Open
Lysosomal trafficking and maturation in neurons remain poorly understood and are unstudied in vivo despite high disease relevance. We generated neuron-specific transgenic mice to track vesicular CTSD acquisition, acidification, and traffic…
View article: Transgenic expression of a ratiometric autophagy probe specifically in neurons enables the interrogation of brain autophagy <i>in vivo</i>
Transgenic expression of a ratiometric autophagy probe specifically in neurons enables the interrogation of brain autophagy <i>in vivo</i> Open
Autophagy-lysosome pathway (ALP) disruption is considered pathogenic in multiple neurodegenerative diseases; however, current methods are inadequate to investigate macroautophagy/autophagy flux in brain in vivo and its therapeutic modulati…