Ferroptosis, a controlled cell death, is driven by iron and characterized by reactive oxygen species and lipid peroxidation. The impact of lipid peroxides, GSH/GPX4, and iron metabolism–targeting small molecule inhibitors is discussed. Nucleic acids, proteins, and phytochemicals are implicated as inhibitors of ferroptosis.
Anwar Ali+10 more
wiley +1 more source
Biomarkers for Huntington's disease: an update [PDF]
Huntington's disease (HD) is a devastating autosomal-dominant neurodegenerative condition caused by a CAG repeat expansion in the gene encoding huntingtin which is characterised by progressive motor impairment, cognitive decline and neuropsychiatric ...
Scahill, RI, Tabrizi, SJ, Wild, EJ
core +1 more source
The Nasal–Brain Drug Delivery Route: Mechanisms and Applications to Central Nervous System Diseases
Τhe BBB restricts CNS drug delivery. NBDD bypasses the BBB via olfactory/trigeminal routes, enabling CNS delivery of therapeutic (small molecules, biologics, nucleic acids) for neurodegenerative/psychiatric disorders and brain tumors using advanced NBDD delivery systems (e.g nanocarriers) to enhance targeting and bioavailability.
Yi Qiu+7 more
wiley +1 more source
Letter to the editor: autoimmune pathogenic mechanisms in Huntington’s disease [PDF]
Letter to the Editor: Autoimmune pathogenic mechanisms in Huntington's ...
DE VINCENTIIS, Marco+5 more
core +1 more source
Polyglutamine expansion induced dynamic misfolding of androgen receptor
Abstract Spinal bulbar muscular atrophy (SBMA) is caused by a polyglutamine expansion (pQe) in the N‐terminal transactivation domain of the human androgen receptor (AR‐NTD), resulting in a combination of toxic gain‐ and loss‐of‐function mechanisms. The structural basis of these processes has not been resolved due to the disordered nature of the NTD ...
Laurens W. H. J. Heling+10 more
wiley +1 more source
Quantification Assays for Total and Polyglutamine-Expanded Huntingtin Proteins
The expansion of a CAG trinucleotide repeat in the huntingtin gene, which produces huntingtin protein with an expanded polyglutamine tract, is the cause of Huntington's disease (HD). Recent studies have reported that RNAi suppression of polyglutamine-expanded huntingtin (mutant HTT) in HD animal models can ameliorate disease phenotypes.
Faywell Albertus+14 more
openaire +5 more sources
ABSTRACT This study aimed to identify key genes associated with post‐chemotherapy recurrence in gastric cancer patients. Gene expression data from multiple cohorts were analysed to determine differentially expressed genes between recurrent and non‐recurrent cases. A prognostic risk model incorporating COL8A1, HSPB7 and SLIT2 was developed and validated
Chao Xu+8 more
wiley +1 more source
Mitochondrial dynamics–fusion, fission, movement, and mitophagy–in neurodegenerative diseases [PDF]
Neurons are metabolically active cells with high energy demands at locations distant from the cell body. As a result, these cells are particularly dependent on mitochondrial function, as reflected by the observation that diseases of mitochondrial ...
Alexander+42 more
core +3 more sources
Reduced Palmitoylation of SQSTM1/p62 in Huntington Disease Is Associated With Impaired Autophagy
Sequestosome 1 (SQSTM1)/p62 is a receptor for autophagy required to deliver damaged organelles and aggregated proteins to the lysosome for degradation. SQSTM1 undergoes palmitoylation, the reversible addition of the saturated fatty acid palmitate to cysteines.
F. Abrar+12 more
wiley +1 more source
Oxidative stress parameters in plasma of Huntington's disease patients, asymptomatic Huntington's disease gene carriers and healthy subjects : a cross-sectional study [PDF]
BACKGROUND : Animal data and postmortem studies suggest a role of oxidative stress in the Huntington's disease (HD), but in vivo human studies have been scarce.
Babić, Tomislav+5 more
core +1 more source