Results 71 to 80 of about 11,293 (160)

Exploring and Targeting the Connection of Iron and Copper Homeostasis to Neurodegenerative Diseases

MedComm, Volume 7, Issue 6, June 2026.
Iron and copper dyshomeostasis, along with their interactions with key intrinsically disordered proteins (e.g., Aβ, tau, α‐synuclein) have a strong implication in the onset and progression of neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), Prion diseases (PrDs), Huntington's disease (HD), Wilson's disease (WD),
Xin Liu, Lin Jia, Kerong Wu, Mo Chen, Jichao Sun, Chuanbin Yang, Chengchao Xu, Jie Sun, Jigang Wang, Lingyun Dai   +9 more
wiley   +1 more source

Polyglutamine Aggregation in Huntington and Related Diseases [PDF]

, 2012
Polyglutamine (polyQ)-expansions in different proteins cause nine neurodegenerative diseases. While polyQ aggregation is a key pathological hallmark of these diseases, how aggregation relates to pathogenesis remains contentious. In this chapter, we review what is known about the aggregation process and how cells respond and interact with the polyQ ...
Polling, S, Hill, AF, Hatters, DM
openaire   +3 more sources

Dendrite injury triggers neuroprotection in Drosophila models of neurodegenerative disease

Scientific Reports
Dendrite defects and loss are early cellular alterations observed across neurodegenerative diseases that play a role in early disease pathogenesis.
Sydney E. Prange, Isha N. Bhakta, Daria Sysoeva, Grace E. Jean, Anjali Madisetti, Hieu H. N. Le, Ly U. Duong, Patrick T. Hwu, Jaela G. Melton, Katherine L. Thompson-Peer   +9 more
doaj   +1 more source

Targeting Mitochondria in Aging‐Related Diseases: Therapeutic Potential and Obstacles

MedComm, Volume 7, Issue 6, June 2026.
This article systematically summarized the specific mechanism of aging‐related diseases caused by mitochondrial dysfunction, and summarized the broad‐spectrum treatment methods and disease targeted treatment strategies for mitochondria. At the same time, it also pointed out the dilemma faced by mitochondrial targeted treatment.
Zijie Xiang, Yu Chen, Xishui Liu, Haowen Lu, Yuqing Yang, Lei Xing, Yu Zhang, Chuandong Lang, Siming Zhang, Shixiang Zhao, Youzhi Hong, Jiaxiang Bai, Yusen Qiao   +12 more
wiley   +1 more source

Modulation of the Stress Granule Component Carhsp1 Mitigates Disease‐Associated Deficits in Spinocerebellar Ataxia Type 3 Mouse Models

Movement Disorders, Volume 41, Issue 6, Page 1516-1527, June 2026.
Abstract Background Spinocerebellar ataxia type 3 (SCA3) is a polyglutamine (polyQ) neurogenerative disorder that results from CAG trinucleotide repeat expansions in the ATXN3 gene, leading to toxic protein aggregate formation and cellular pathway dysfunction.
Tiago Moreira‐Gomes, Adriana Marcelo, Ana Teresa Rajado, Rafael G. Costa, Ricardo Afonso‐Reis, Cristiana R. Madeira, Inês T. Afonso, David V.C. Brito, Adriana A. Vaz, Clévio Nóbrega   +9 more
wiley   +1 more source

Lipid composition controls the huntingtin exon 1 membrane‐association and differentially modulates its flanking regions' dynamics

Protein Science, Volume 35, Issue 6, June 2026.
Abstract The pathological expansion of the polyglutamine (polyQ) repeat within the first exon of huntingtin (Httex1) protein is a defining hallmark of Huntington's disease (HD). Multiple evidence supports that the membrane recruitment of Httex1 is critical for its self‐assembly and related toxicity in HD.
Tânia Sousa, Gonçalo Damas, Ana Coutinho, Nuno Bernardes, Ana Azevedo, Manuel Prieto, Ana M. Melo   +6 more
wiley   +1 more source

RNA therapy for polyglutamine neurodegenerative diseases

Expert Reviews in Molecular Medicine, 2012
Polyglutamine neurodegenerative diseases result from the expansion of a trinucleotide CAG repeat, encoding a polyglutamine tract in the disease-causing protein. The process by which each polyglutamine protein exerts its toxicity is complex, involving a variety of mechanisms including transcriptional dysregulation, proteasome impairment and ...
Watson, L, Wood, M
openaire   +3 more sources

Redox environment modulates aggregation of ataxin‐3 in vitro — Implications for drug screening of cysteine‐rich proteins

The FEBS Journal, Volume 293, Issue 11, Page 3376-3398, June 2026.
Redox environment modulates in vitro aggregation of Ataxin‐3, the protein implicated in spinocerebellar ataxia type 3. Reducing conditions stabilize native monomers and prevent aggregation, whereas oxidative conditions promote the formation of non‐native conformers and disulfide‐linked oligomers within the Josephin domain (JD).
Martyna Podlasiak, Martina Sollazzo, Elisa Monaca, Raffaele Sabbatella, Maria Agnese Morando, Oleg Chertkov, Laura Puglisi, Martina Mascellino, Anna Fricano, Sandra Macedo‐Ribeiro, Caterina Alfano   +10 more
wiley   +1 more source

Detection of ubiquitinated huntingtin species in intracellular aggregates

Frontiers in Molecular Neuroscience, 2015
Protein conformation diseases, including polyglutamine diseases, result from the accumulation and aggregation of misfolded proteins. Huntington’s disease is one of nine diseases caused by an expanded polyglutamine repeat within the affected protein and ...
Katrin eJuenemann, Anne eWiemhoefer, Eric eReits   +2 more
doaj   +1 more source

Caloric restriction blocks neuropathology and motor deficits in Machado–Joseph disease mouse models through SIRT1 pathway

Nature Communications, 2016
SIRTs have been reported to provide neuroprotective actions in polyglutamine diseases, and are linked to the beneficial effects of caloric restrictive diets.
Janete Cunha-Santos, Joana Duarte-Neves, Vitor Carmona, Leonard Guarente, Luís Pereira de Almeida, Cláudia Cavadas   +5 more
doaj   +1 more source