Aβ42 promotes the aggregation of α‐synuclein splice isoforms via heterogeneous nucleation
The aggregation of amyloid‐β (Aβ) and α‐synuclein (αSyn) is associated with Alzheimer's and Parkinson's diseases. This study reveals that Aβ aggregates serve as potent nucleation sites for the aggregation of αSyn and its splice isoforms, shedding light on the intricate interplay between these two pathogenic proteins.
Alexander Röntgen+2 more
wiley +1 more source
The Cellular and Subcellular Localization of Huntingtin-Associated Protein 1 (HAP1): Comparison with Huntingtin in Rat and Human [PDF]
The cellular and subcellular distribution of HAP1 was examined in rat brain by light and electron microscopic immunocytochemistry and subcellular fractionation. HAP1 localization was also determined in human postmortem tissue from control and Huntington’s disease (HD) cases by light microscopic immunocytochemistry.
Hong Yi+5 more
openaire +3 more sources
Stage‐Dependent Inhibitory Connectivity in Striatal‐Motor Circuit in Huntington's Disease
ABSTRACT Background Elucidating dysfunctional connectivity patterns among key brain regions in Huntington's disease (HD) underlying progression may have implications for developing treatment and therapeutic evaluation. Objective Explore the relationship between abnormal spontaneous resting‐state activity and atrophy in HD‐specific brain regions and ...
Yinghua Jing+4 more
wiley +1 more source
Huntington's disease: An immune perspective [PDF]
Copyright © 2011 Annapurna Nayaketal. This article has been made available through the Brunel Open Access Publishing Fund.Huntington's disease (HD) is a progressive neurodegenerative disorder that is caused by abnormal expansion of CAG trinucleotide ...
Ansar, R+4 more
core +3 more sources
scyllo-Inositol Promotes Robust Mutant Huntingtin Protein Degradation*
Background: Effects of scyllo-inositol, a modulator of misfolded protein accumulation, were tested in a cellular model of Huntington disease. Results: scyllo-Inositol lowered mutant huntingtin aggregation and decreased protein abundance through ...
A. Lai+4 more
semanticscholar +1 more source
Extracellular vesicles (EVs) play a dual role in diagnostics and therapeutics, offering innovative solutions for treating cancer, cardiovascular, neurodegenerative, and orthopedic diseases. This review highlights EVs’ potential to revolutionize personalized medicine through specific applications in disease detection and treatment.
Farbod Ebrahimi+4 more
wiley +1 more source
Stimulation of S1PR5 with A-971432, a selective agonist, preserves blood-brain barrier integrity and exerts therapeutic effect in an animal model of Huntington's disease [PDF]
Huntington's disease (HD) is themost common neurodegenerative disorder for which no effective cure is yet available. Although several agents have been identified to provide benefits so far, the number of therapeutic options remains limited with only ...
Amico, Enrico+11 more
core +1 more source
Rewiring Neuroimmunity: Nanoplatform Innovations for CNS Disease Therapy
This review explores emerging nanoplatform strategies designed to modulate neuroimmune responses for treating central nervous system (CNS) disorders. It examines structural and microenvironmental barriers, advances in multifunctional and targeted nanotechnologies, and highlights clinical progress and translational challenges, offering insights into the
Muhammad Usman Akbar+7 more
wiley +1 more source
Effects of flanking sequences and cellular context on subcellular behavior and pathology of mutant HTT [PDF]
Huntington’s disease (HD) is caused by an expansion of a poly glutamine (polyQ) stretch in the huntingtin protein (HTT) that is necessary to cause pathology and formation of HTT aggregates.
Agrawal, Namita+10 more
core
PAK in Alzheimer disease, Huntington disease and X-linked mental retardation. [PDF]
Developmental cognitive deficits including X-linked mental retardation (XLMR) can be caused by mutations in P21-activated kinase 3 (PAK3) that disrupt actin dynamics in dendritic spines.
Cole, Greg M+3 more
core +1 more source