Biphasic Temporal Remodeling Of The Proteome In A Polyglutamine-Expanded Huntingtin In Vitro Aggregation Cell Model: From Early Rna-Regulatory Compensation To Selective Mitochondrial Energy Failure
Findings define a biphasic course of huntingtin toxicity and highlight an early therapeutic window in which intervention is most likely to be applied, prior to irreversible deterioration of mitochondrial respiratory function.
Huntington's disease (HD) offers a particularly instructive, if sobering, window into what happens when a cell's protein-clearance machinery is asked to do more than it can bear. Background: the ubiquitin-proteasome system (UPS) is the principal route by which short-lived and misfolded proteins are removed from eukaryo...
How dynamic changes in IRE1α signaling bias contribute to amyloidogenic progression in AD is examined and whether selective modulation of adaptive versus maladaptive IRE1α outputs may offer stage-dependent therapeutic benefit is considered.
Dan-Yun Wang, Qinan Yin· Frontiers in Molecular Biosc...· 0 citations
Progressive mitochondrial dysfunction coupled with calcium dyshomeostasis is a hallmark of aging and neurodegenerative conditions, yet the molecular links to cognitive decline remain unclear. Moreover, although sex differences in susceptibility to neurodegeneration are well recognized, their molecular basis remains poo...
Sergey V. Ivanov, Victor Paromov, M. Aksu et al.· Mechanisms of Ageing and Dev...· 0 citations
A physiologically relevant human model is established that separates early TDP-43 toxic gain-of-function from basal loss-of-function from basal loss-of-function while providing a robust platform for investigating TDP-43 biology and accelerating therapeutic discovery in ALS.
M. Cicardi, Sara Antonini, Ivette Martorell Serra et al.· bioRxiv· 0 citations
Huntington's disease (HD) is a life-threatening neurodegenerative disease caused by a mutation in Huntingtin (HTT). Neuropathology in HD is marked by a progressive loss of neurons in the caudate putamen and the deposition of mutant HTT aggregates as cytoplasmic and nuclear inclusions. At present, no disease-modifying t...
An Wu, Xue-Yi Li· Journal of Huntington's Dise...· 0 citations
It is reported that T‑2 toxin remodels APP and Tau homeostasis, featuring an early decrease in full‑length APP and a delayed, sustained increase in Tau phosphorylation and total Tau, accompanied by dynamic cytokine release.
Tong Nie, Junya Li, Shiqing Tan et al.· Neurotoxicology· 0 citations
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