keyword
https://read.qxmd.com/read/38463392/non-coding-rnas-and-neuroinflammation-implications-for-neurological-disorders
#21
REVIEW
Yvonne Chen, Julia Mateski, Linda Gerace, Jonathan Wheeler, Jan Burl, Bhavna Prakash, Cherie Svedin, Rebecca Amrick, Brian D Adams
Neuroinflammation is considered a balanced inflammatory response important in the intrinsic repair process after injury or infection. Under chronic states of disease, injury, or infection, persistent neuroinflammation results in a heightened presence of cytokines, chemokines, and reactive oxygen species that result in tissue damage. In the CNS, the surrounding microglia normally contain macrophages and other innate immune cells that perform active immune surveillance. The resulting cytokines produced by these macrophages affect the growth, development, and responsiveness of the microglia present in both white and gray matter regions of the CNS...
2024: Experimental Biology and Medicine
https://read.qxmd.com/read/38462589/dysregulation-of-extracellular-potassium-distinguishes-healthy-ageing-from-neurodegeneration
#22
JOURNAL ARTICLE
Fengfei Ding, Qian Sun, Carter Long, Rune Nguyen Rasmussen, Sisi Peng, Qiwu Xu, Ning Kang, Wei Song, Pia Weikop, Steven A Goldman, Maiken Nedergaard
Progressive neuronal loss is a hallmark feature distinguishing neurodegenerative diseases from normal aging. However, the underlying mechanisms remain unknown. Extracellular K+ homeostasis is a potential mediator of neuronal injury since K+ elevations increase excitatory activity. The dysregulation of extracellular K+ and potassium channel expressions during neurodegeneration could contribute to this distinction. We here measured the cortical extracellular K+ concentration ([K+]e) in awake wildtype mice as well as murine models of neurodegeneration using K+-sensitive microelectrodes...
March 11, 2024: Brain
https://read.qxmd.com/read/38461512/alterations-in-cerebrospinal-fluid-urea-occur-in-late-manifest-huntington-s-disease
#23
JOURNAL ARTICLE
Anna C Pfalzer, Shuhei Shiino, James Silverman, Simona G Codreanu, Stacy D Sherrod, John A McLean, Daniel O Claassen
BACKGROUND: Huntington's disease (HD) is a neurodegenerative disorder caused by expanded cytosine-adenine-guanine (CAG) repeats in the Huntingtin gene, resulting in the production of mutant huntingtin proteins (mHTT). Previous research has identified urea as a key metabolite elevated in HD animal models and postmortem tissues of HD patients. However, the relationship between disease course and urea elevations, along with the molecular mechanisms responsible for these disturbances remain unknown...
March 2, 2024: Journal of Huntington's Disease
https://read.qxmd.com/read/38460902/glycine-transporter-1-inhibition-by-nfps-promotes-neuroprotection-against-striatal-damage-models
#24
JOURNAL ARTICLE
Raul Izidoro Ribeiro, Gustavo Almeida Carvalho, Raphaela Almeida Chiareli, Isabel Vieira de Assis Lima, Paula Maria Quaglio Bellozi, Onésia Cristina Oliveira-Lima, Ágatha Oliveira Giacomelli, Alexander Birbrair, Renato Santiago Gomez, Antônio Carlos Pinheiro de Oliveira, Henning Ulrich, Mauro Cunha Xavier Pinto
The striatum, an essential component of the brain's motor and reward systems, plays a pivotal role in a wide array of cognitive processes. Its dysfunction is a hallmark of neurodegenerative diseases like Parkinson's disease (PD) and Huntington's disease (HD), leading to profound motor and cognitive deficits. These conditions are often related to excitotoxicity, primarily due to overactivation of NMDA receptors (NMDAR). In the synaptic cleft, glycine transporter type 1 (GlyT1) controls the glycine levels, a NMDAR co-agonist, which modulates NMDAR function...
March 7, 2024: Neuroscience Letters
https://read.qxmd.com/read/38459557/tyrobp-dap12-knockout-in-huntington-s-disease-q175-mice-cell-autonomously-decreases-microglial-expression-of-disease-associated-genes-and-non-cell-autonomously-mitigates-astrogliosis-and-motor-deterioration
#25
JOURNAL ARTICLE
Jordi Creus-Muncunill, Jean Vianney Haure-Mirande, Daniele Mattei, Joanna Bons, Angie V Ramirez, B Wade Hamilton, Chuhyon Corwin, Sarah Chowdhury, Birgit Schilling, Lisa M Ellerby, Michelle E Ehrlich
INTRODUCTION: Huntington's disease (HD) is a fatal neurodegenerative disorder caused by an expansion of the CAG trinucleotide repeat in the Huntingtin gene (HTT). Immune activation is abundant in the striatum of HD patients. Detection of active microglia at presymptomatic stages suggests that microgliosis is a key early driver of neuronal dysfunction and degeneration. Recent studies showed that deletion of Tyrobp, a microglial protein, ameliorates neuronal dysfunction in Alzheimer's disease amyloidopathy and tauopathy mouse models while decreasing components of the complement subnetwork...
March 8, 2024: Journal of Neuroinflammation
https://read.qxmd.com/read/38459427/huntingtin-htt1a-is-generated-in-a-cag-repeat-length-dependent-manner-in-human-tissues
#26
JOURNAL ARTICLE
Franziska Hoschek, Julia Natan, Maximilian Wagner, Kirupa Sathasivam, Alshaimaa Abdelmoez, Björn von Einem, Gillian P Bates, G Bernhard Landwehrmeyer, Andreas Neueder
BACKGROUND: The disease-causing mutation in Huntington disease (HD) is a CAG trinucleotide expansion in the huntingtin (HTT) gene. The mutated CAG tract results in the production of a small RNA, HTT1a, coding for only exon 1 of HTT. HTT1a is generated by a block in the splicing reaction of HTT exon 1 to exon 2 followed by cleavage in intron 1 and polyadenylation. Translation of HTT1a leads to the expression of the highly toxic HTT exon 1 protein fragment. We have previously shown that the levels of HTT1a expression in mouse models of HD is dependent on the CAG repeat length...
March 8, 2024: Molecular Medicine
https://read.qxmd.com/read/38454250/a-case-of-chorea-with-slow-saccades-caused-by-nkx2-1-mutation
#27
JOURNAL ARTICLE
Johanna Vercammen, Joke Terryn, Sien Van Daele, Sascha Vermeer, Wim Vandenberghe
No abstract text is available yet for this article.
March 7, 2024: Movement Disorders Clinical Practice
https://read.qxmd.com/read/38453033/agmatine-mitigates-behavioral-abnormalities-and-neurochemical-dysregulation-associated-with-3-nitropropionic-acid-induced-huntington-s-disease-in-rats
#28
JOURNAL ARTICLE
Raj Katariya, Kartikey Mishra, Shivkumar Sammeta, Milind Umekar, Nandkishor Kotagale, Brijesh Taksande
Huntington's disease (HD) is a progressive neurodegenerative condition characterized by a severe motor incoordination, cognitive decline, and psychiatric complications. However, a definitive cure for this devastating disorder remains elusive. Agmatine, a biogenic amine, has gain attention for its reported neuromodulatory and neuroprotective properties. The present study was designed to examine the influence of agmatine on the behavioral, biochemical, and molecular aspects of HD in an animal model. A mitochondrial toxin, 3-nitro propionic acid (3-NP), was used to induce HD phenotype and similar symptoms such as motor incoordination, memory impairment, neuro-inflammation, and depressive-like behavior in rats...
March 5, 2024: Neurotoxicology
https://read.qxmd.com/read/38450912/disentangling-the-neurobiological-bases-of-temporal-impulsivity-in-huntington-s-disease
#29
JOURNAL ARTICLE
Helena Pardina-Torner, Audrey E De Paepe, Clara Garcia-Gorro, Nadia Rodriguez-Dechicha, Irene Vaquer, Matilde Calopa, Jesus Ruiz-Idiago, Celia Mareca, Ruth de Diego-Balaguer, Estela Camara
BACKGROUND: Despite its impact on daily life, impulsivity in Huntington's disease (HD) is understudied as a neuropsychiatric symptom. Our aim is to characterize temporal impulsivity in HD and to disentangle the white matter correlate associated with impulsivity. METHODS: Forty-seven HD individuals and 36 healthy controls were scanned and evaluated for temporal impulsivity using a delay-discounting (DD) task and complementary Sensitivity to Punishment and Sensitivity to Reward Questionnaire...
March 2024: Brain and Behavior
https://read.qxmd.com/read/38450553/assessment-of-fitbit-charge-4-for-sleep-stage-and-heart-rate-monitoring-against-polysomnography-and-during-home-monitoring-in-huntington-s-disease
#30
JOURNAL ARTICLE
Emer P Doheny, Klavs Renerts, Andreas Braun, Esther Werth, Christian Baumann, Philipp Baumgartner, Philippa Morgan-Jones, Monica Busse, Madeleine M Lowery, Hans H Jung
STUDY OBJECTIVES: Wearable devices, monitoring sleep stages and heart rate (HR), bring the potential for longitudinal sleep monitoring in patients with neurodegenerative diseases. Sleep quality reduces with disease progression in Huntington's disease (HD). However, the involuntary movements characteristic of HD may affect the accuracy of wrist-worn devices. This study compares sleep stage and heart rate data from the Fitbit Charge 4 (FB) against polysomnography (PSG) in participants with HD...
March 7, 2024: Journal of Clinical Sleep Medicine: JCSM: Official Publication of the American Academy of Sleep Medicine
https://read.qxmd.com/read/38449715/repeating-themes-of-plastic-genes-and-therapeutic-schemes-targeting-the-tandem-repeatome
#31
JOURNAL ARTICLE
Anthony J Hannan
This scientific commentary refers to 'Modification of Huntington's disease by short tandem repeats' by Hong et al . (https://doi.org/10.1093/braincomms/fcae016) in Brain Communications .
2024: Brain communications
https://read.qxmd.com/read/38449714/modification-of-huntington-s-disease-by-short-tandem-repeats
#32
JOURNAL ARTICLE
Eun Pyo Hong, Eliana Marisa Ramos, N Ahmad Aziz, Thomas H Massey, Branduff McAllister, Sergey Lobanov, Lesley Jones, Peter Holmans, Seung Kwak, Michael Orth, Marc Ciosi, Vilija Lomeikaite, Darren G Monckton, Jeffrey D Long, Diane Lucente, Vanessa C Wheeler, Tammy Gillis, Marcy E MacDonald, Jorge Sequeiros, James F Gusella, Jong-Min Lee
Expansions of glutamine-coding CAG trinucleotide repeats cause a number of neurodegenerative diseases, including Huntington's disease and several of spinocerebellar ataxias. In general, age-at-onset of the polyglutamine diseases is inversely correlated with the size of the respective inherited expanded CAG repeat. Expanded CAG repeats are also somatically unstable in certain tissues, and age-at-onset of Huntington's disease corrected for individual HTT CAG repeat length (i.e. residual age-at-onset), is modified by repeat instability-related DNA maintenance/repair genes as demonstrated by recent genome-wide association studies...
2024: Brain communications
https://read.qxmd.com/read/38447791/ribosome-profiling-and-mass-spectrometry-reveal-widespread-mitochondrial-translation-defects-in-a-striatal-cell-model-of-huntington-disease
#33
JOURNAL ARTICLE
Sunayana Dagar, Manish Sharma, George Tsaprailis, Catherina Scharager Tapia, Gogce Crynen, Preksha Sandipkumar Joshi, Neelam Shahani, Srinivasa Subramaniam
Huntington disease (HD) is caused by an expanded polyglutamine mutation in huntingtin (mHTT) that promotes prominent atrophy in the striatum and subsequent psychiatric, cognitive, and choreiform movements. Multiple lines of evidence point to an association between HD and aberrant striatal mitochondrial functions; however, the present knowledge about whether (or how) mitochondrial mRNA translation is differentially regulated in HD remains unclear. We found that protein synthesis is diminished in HD mitochondria compared to healthy control striatal cell models...
March 4, 2024: Molecular & Cellular Proteomics: MCP
https://read.qxmd.com/read/38447638/understanding-of-referential-dependencies-in-huntington-s-disease
#34
JOURNAL ARTICLE
Antonia Tovar, Scott James Perry, Esteban Muñoz, Celia Painous, Pilar Santacruz, Jesús Ruiz-Idiago, Celia Mareca, Wolfram Hinzen
No abstract text is available yet for this article.
March 5, 2024: Neuropsychologia
https://read.qxmd.com/read/38444595/neuroimmune-pathways-involvement-in-neurodegeneration-of-r6-2-mouse-model-of-huntington-s-disease
#35
JOURNAL ARTICLE
Emanuela Paldino, Giorgia Migliorato, Francesca R Fusco
Mechanisms of tissue damage in Huntington's disease (HD) involve excitotoxicity, mitochondrial damage, and neuroinflammation, including microglia activation. CD47 is a membrane protein that interacts with the inhibitory immunoreceptor SIRPα. Engagement of SIRPα by CD47 provides a downregulatory signal that inhibits host cell phagocytosis, promoting a "don't-eat-me" signal. These proteins are involved in the immune response and are downmodulated in inflammatory diseases. The involvement of inflammation and of the inflammasome in HD has already been described...
2024: Frontiers in Cellular Neuroscience
https://read.qxmd.com/read/38442614/investigating-the-binding-interaction-of-quinoline-yellow-with-bovine-serum-albumin-and-anti-amyloidogenic-behavior-of-ferulic-acid-on-qy-induced-bsa-fibrils
#36
JOURNAL ARTICLE
Maham Fatima, Faisal Nabi, Rizwan Hasan Khan, Aabgeena Naeem
Protein aggregation induces profound changes in the structure along with the conformation of the protein, and is responsible for the pathogenesis of a number of neurodegenerative conditions such as Huntington's, Creutzfeldt-Jacob, Type II diabetes mellitus, Alzheimer's, etc. Numerous multi-spectroscopic approaches and in-silico experiments were utilized to investigate BSA's biomolecular interaction and aggregation in the presence of quinoline yellow. The present research investigation evaluated the interaction of BSA with the food colorant (QY) at two different pH (7...
February 25, 2024: Spectrochimica Acta. Part A, Molecular and Biomolecular Spectroscopy
https://read.qxmd.com/read/38441722/involvement-of-autophagic-machinery-in-neuropathogenesis-targeting-and-relevant-methods-of-detection
#37
JOURNAL ARTICLE
Nourhan Sayed, Alaa Emam Ali, Doaa Mokhtar Elsherbiny, Samar S Azab
The exquisite balance between cellular prosurvival and death pathways is extremely necessary for homeostasis. Different forms of programmed cell death have been widely studied and reported such as apoptosis, necroptosis, pyroptosis, and autophagy. Autophagy is a catabolic process important for normal cellular functioning. The main aim of this machinery is to degrade the misfolded or damaged proteins, unuseful organelles, and pathogens, which invade the cells, thereby maintaining cellular homeostasis and assuring the regular renewal of cell components...
March 6, 2024: Methods in Molecular Biology
https://read.qxmd.com/read/38441007/cross-talks-between-cns-and-cvs-diseases-an-alliance-to-annihilate
#38
JOURNAL ARTICLE
Shivani Chib, Sushma Devi, Rishabh Chalotra, Neeraj Mittal, Thakur Gurjeet Singh, Puneet Kumar, Randhir Singh
Cardiovascular and neurological diseases cause substantial morbidity and mortality globally. Moreover, cardiovascular diseases are the leading cause of death globally. About 17.9 million people are affected by cardiovascular diseases and 6.8 million people die every year due to neurological diseases. The common neurologic manifestations of cardiovascular illness include stroke syndrome which is responsible for unconsciousness and several other morbidities significantly diminished the quality of life of patients...
March 4, 2024: Current Cardiology Reviews
https://read.qxmd.com/read/38436789/cardiac-autonomic-involvement-in-huntington-s-disease
#39
JOURNAL ARTICLE
Dilek İşcan, Yakup Çetinkaya
INTRODUCTION: Huntington's disease (HD) is known as a neurodegenerative disease with movement disorder and cognitive impairment; autonomic involvement is also becoming common in some recent studies. The aim of this study is to demonstrate the presence of cardiac autonomic involvement in HD patients. METHOD: Time and frequency domain parameters obtained from the 24-h Holter ECG(hECG) were compared between 20 HD patients and 20 healthy control subjects. RESULTS: Fourteen HD patients had tachycardia, bradycardia, and extra beats...
March 4, 2024: Neurological Sciences
https://read.qxmd.com/read/38434042/disrupted-nuclear-import-of-cell-cycle-proteins-in-huntington-s-polyq-disease-causes-neurodevelopment-defects-in-cellular-and-drosophila-model
#40
JOURNAL ARTICLE
Sandeep Kumar Dubey, Thomas E Lloyd, Madhu G Tapadia
Huntington's disease is caused by an expansion of CAG repeats in exon 1 of the huntingtin gene encoding an extended PolyQ tract within the Huntingtin protein (mHtt). This expansion results in selective degeneration of striatal medium spiny projection neurons in the basal ganglia. The mutation causes abnormalities during neurodevelopment in human and mouse models. Here, we report that mHtt/PolyQ aggregates inhibit the cell cycle in the Drosophila brain during development. PolyQ aggregates disrupt the nuclear pore complexes of the cells preventing the translocation of cell cycle proteins such as Cyclin E, E2F and PCNA from cytoplasm to the nucleus, thus affecting cell cycle progression...
February 29, 2024: Heliyon
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