Results 111 to 120 of about 40,748 (225)

Emerging Therapies for Huntington’s Disease – Focus on N-Terminal Huntingtin and Huntingtin Exon 1

Biologics: Targets & Therapy, 2022
M Leontien van der Bent, Melvin M Evers, Astrid Vallès uniQure biopharma B.V., Department of Research and Development, Amsterdam, the NetherlandsCorrespondence: Astrid Vallès, uniQure biopharma B.V, Postbus 22506, Amsterdam, 1100 DA, the Netherlands, Tel
van der Bent ML, Evers MM, Vallès A
doaj  

Cilia in Nervous System Development, Function, and Disease

MedComm – Future Medicine, Volume 5, Issue 2, June 2026.
Cilia are evolutionarily conserved organelles that function as essential sensory and motility platforms in the nervous system. This review outlines key cilia‐dependent signaling pathways and their roles in neural development and function. Furthermore, it highlights how ciliary dysfunction can lead to a variety of neurological disorders, known as ...
Qingchao Li, Anqi Zhang, Ting Song
wiley   +1 more source

Multiple discrete soluble aggregates influence polyglutamine toxicity in a Huntington\u27s disease model system [PDF]

, 2016
Huntington’s disease (HD) results from expansions of polyglutamine stretches (polyQ) in the huntingtin protein (Htt) that promote protein aggregation, neurodegeneration, and death.
Denis, Clyde L., Wang, Xin, Xi, Wen
core   +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

The kynurenine pathway as a therapeutic target in cognitive and neurodegenerative disorders [PDF]

, 2013
Understanding the neurochemical basis for cognitive function is one of the major goals of neuroscience, with a potential impact on the diagnosis, prevention and treatment of a range of psychiatric and neurological disorders.
Akagbosu, Akladios, Alexander, Alkondon, Alkondon, Alkondon, Amori, Andersen, Atlas, Autier, Backman, Beal, Benatti, Bonda, Breese, Carpenedo, Carpenedo, Casazza, Castellano, Ceresoli-Borroni, Cesura, Chess, Chess, Chess, Chiarugi, Chiarugi, Clark, Cochran, Cozzi, Cui, Daily, Dalley, Dantzer, Darlington, Darlington, Davidson, Deiana, Della Torre, DiNatale, Dobelis, Dounay, Eastman, Erhardt, Forrest, Forrest, Forrest, Forrest, Fukui, Gellert, Giordani, Giorgini, Gold, Graef, Guidetti, Guidetti, Guidetti, Guidetti, Guillemin, Guillemin, Hardingham, Hedges, Henderson, Heng, Hernandez, Heyes, Hilmas, Holtze, Jason, Jauch, Jentsch, Jurgens, Kalisch, Kandanearatchi, Kiank, Kihara, Kloet, Kocki, Konradsson-Geuken, Lawrence, Lawrence, Linderholm, Lindsley, Luchowski, Luchowski, Lupien, Marin, Mexal, Millan, Miller, Minzenberg, Miura, Moeller, Mok, Muchowski, Muchowski, Mueller, Muscatell, Myint, Nagy, Neill, Newcomer, Newcomer, Nilsson, Nilsson, Nozaki, O'Connor, Olsson, Onur, Owe-Young, Paterson, Pearson, Pechtel, Pellicciari, Pellicciari, Perkins, Pertovaara, Pevarello, Phillips, Pocivavsek, Pocivavsek, Popoli, Popoli, Potter, Rahman, Raison, Rassoulpour, Ren, Robert, Rodgers, Rossi, Ryu, Röver, Saito, Salazar, Sapko, Sarter, Sathyasaikumar, Sathyasaikumar, Schwarcz, Schwarcz, Schwarcz, Schwarcz, Shear, Speciale, Speciale, Stazka, Stazka, Stone, Stone, Stone, Stone, Stone, Stoy, Tadaiesky, Tatter, Teichberg, Teichberg, Ting, Trecartin, Tse, Varasi, Vezzani, Walker, Wang, Wang, Wejksza, Wejksza, Wonodi, Xu, Yamada, Yuen, Zisapel, Zmarowski   +172 more
core   +1 more source

Unraveling the Dynamics of Oxytocin in Hypothalamic Neurons

Traffic, Volume 27, Issue 2, June 2026.
Oxytocin (OT) plays an important role in regulating social behavior, and dysregulation of the oxytocinergic system leads to social impairments, such as autism spectrum disorder. Central OT release is poorly understood. Using live‐cell imaging to track vesicle trajectories, combined with machine learning‐based classification, the analysis reveals ...
Beatriz Aznar‐Escolano, Vera Egorova, José Villanueva, Luis Miguel Gutiérrez, Virginia González‐Vélez, Amparo Gil, Sandra Jurado   +6 more
wiley   +1 more source

Identification of Binding Sites in Huntingtin for the Huntingtin Interacting Proteins HIP14 and HIP14L

PLoS ONE, 2014
Huntington disease is an adult onset neurodegenerative disease characterized by motor, cognitive, and psychiatric dysfunction, caused by a CAG expansion in the HTT gene. Huntingtin Interacting Protein 14 (HIP14) and Huntingtin Interacting Protein 14-like (HIP14L) are palmitoyl acyltransferases (PATs), enzymes that mediate the post-translational ...
Shaun S Sanders, Katherine K N Mui, Liza M Sutton, Michael R Hayden   +3 more
openaire   +4 more sources

Discovery and Targeted Proteomic Studies Reveal Striatal Markers Validated for Huntington's Disease

Annals of Clinical and Translational Neurology, Volume 13, Issue 5, Page 911-923, May 2026.
ABSTRACT Objective Clinical trials for Huntington's disease (HD) enrolling persons before clinical motor diagnosis (CMD) lack validated biomarkers. This study aimed to conduct an unbiased discovery analysis and a targeted examination of proteomic biomarkers scrutinized by clinical validation. Methods Cerebrospinal fluid was obtained from PREDICT‐HD and
Daniel Chelsky, Cara Joyce, H. Jeremy Bockholt, Paul A. Rudnick, William H. Adams, Fiona McAllister, Justin W. Smock, Michael A. Newton, Jane S. Paulsen   +8 more
wiley   +1 more source

Mutant Huntingtin Forms in Vivo Complexes with Distinct Context-Dependent Conformations of the Polyglutamine Segment

Neurobiology of Disease, 1999
Huntington's disease (HD) is caused by an expanded glutamine tract, which confers a novel aggregation-promoting property on the 350-kDa huntingtin protein.
Francesca Persichetti, Flavia Trettel, C.Chris Huang, Cornel Fraefel, H.T.Marc Timmers, James F. Gusella, Marcy E. MacDonald   +6 more
doaj   +1 more source

IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosome [PDF]

, 2009
Expansion of the polyglutamine repeat within the protein Huntingtin (Htt) causes Huntington's disease, a neurodegenerative disease associated with aging and the accumulation of mutant Htt in diseased neurons.
Aiken, Ali Khoshnan, Alice L. Lau, Ana Maria Cuervo, Anne, Apostol, Arrasate, Arrasate, Ashish Massey, Atwal, Atwal, Björkqvist, Brown, Charity T. Aiken, Chen, Chondrogianni, Cornett, Cuervo, Cuervo, Cuervo, D'Orazi, Dan, Donald C. Lo, Fang, Finkbeiner, Frank M. LaFerla, Gillian Bates, Graham, Grossman, Gu, Guerrero, Gutekunst, Hasan Khashwji, Henn, Hernandez-Hernandez, Hietakangas, Hofmann, Hu, Huang, Humbert, Hunter, J. Lawrence Marsh, Jacqueline Gire O'Rourke, Jeong, Jiang, Joan S. Steffan, Karin, Karin, Katalin Illes, Kaushik, Kazantsev, Khoshnan, Khoshnan, Kim N. Green, Komatsu, Lan Huang, Leslie Michels Thompson, Linda S. Kaltenbach, Liu, Lo, Luo, Mangiarini, Marta Martinez-Vincente, Martinez-Vicente, Massey, Massey, Michael R. Hayden, Michels, Mizushima, Montserrat Arrasate, Namita Agrawal, Orr, Paul H. Patterson, Peters-Libeu, Rockabrand, Saudou, Schilling, Scott O. Zeitlin, Shao, Southwell, Steffan, Steffan, Steffan, Steven Finkbeiner, Tagwerker, Tamas Lukacsovich, Tonoki, Verma, Walker, Warby, Warby, Warby, Wu, Xia, Ya-Zhen Zhu, Yanai, Zhang, Zuccato   +97 more
core   +3 more sources