Results 111 to 120 of about 19,593 (221)

Neuro‐Immune Crosstalk: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets

MedComm, Volume 7, Issue 2, February 2026.
Neurons, immune cells, and other cellular components within the disease microenvironment (such as stromal cells and tumor cells) constitute a dynamically evolving ecosystem. Neurons directly modulate immune cell activity and inflammatory responses through the release of neurotransmitters (e.g., norepinephrine and CGRP), while also promoting tumor ...
Xin Guo, Hui Liu, Yu‐Jing Song, Jian‐Hua Wang, Danfeng Liu, Zhi‐Wei Zheng, Jia‐Jun Li, Boya Li, An Song, Wei He, Lei‐Lei Yang, Shuo Wang   +11 more
wiley   +1 more source

Frustration Between Preferred States of Complementary Trinucleotide Repeat DNA Hairpins Anticorrelates with Expansion Disease Propensity [PDF]

, 2023
Pengning Xu, Jiahui Zhang, Feng Pan, Chelsea Mahn, Christopher Roland, Celeste Sagui, Keith Weninger   +6 more
openalex   +1 more source

P53 binds preferentially to non-B DNA structures formed by the pyrimidine-rich strands of GaA·TTC trinucleotide repeats associated with Friedreich’s ataxia [PDF]

, 2019
Expansions of trinucleotide repeats (TNRs) are associated with genetic disorders such as Friedreich’s ataxia. The tumor suppressor p53 is a central regulator of cell fate in response to different types of insults.
Adámik, Matej, Bažantová, Pavla, Bowater, Richard P., Brázdová, Marie, Fojta, Miroslav, Helma, Robert, Pastuchová, Alena, Petr, Marek, Pečinka, Petr, Renčiuk, Daniel, Soldánová, Zuzana, Tichý, Vlastimil   +11 more
core   +1 more source

Discovery of disrupted sustained attention and altered functional connectivity in far‐from‐onset Huntington's disease gene‐expanded young adults

Alzheimer's &Dementia, Volume 22, Issue 1, January 2026.
Abstract BACKGROUND Cognitive impairments are a hallmark of Huntington's disease (HD). METHODS Seventy‐one participants (43 HD gene‐expanded [HDGE], 28 healthy controls) from the HD‐Young Adult Study at two timepoints ≈ 4.7 years apart, completed the Cambridge Neuropsychological Test Automated Battery Rapid Visual Information Processing task and ...
Christelle Langley, Michela Leocadi, Nicola Z. Hobbs, Mena Farag, Michael J. Murphy, Kate Fayer, Rachael I. Scahill, James B. Rowe, Trevor W. Robbins, Sarah J. Tabrizi, Barbara J. Sahakian   +10 more
wiley   +1 more source

Ethidium Bromide Modifies The Agarose Electrophoretic Mobility of CAG•CTG Alternative DNA Structures Generated by PCR

Frontiers in Cellular Neuroscience, 2017
The abnormal expansion of unstable simple sequence DNA repeats can cause human disease through a variety of mechanisms, including gene loss-of-function, toxic gain-of-function of the encoded protein and toxicity of the repeat-containing RNA transcript ...
Mário Gomes-Pereira, Mário Gomes-Pereira, Darren G. Monckton   +2 more
doaj   +1 more source

Genetically confirmed first Indian dentatorubral–pallidoluysian atrophy kindred: A case report

Annals of Movement Disorders, 2020
DRPLA (dentatorubral–pallidoluysian atrophy) is a neurodegenerative disorder caused by cytosine-adenine-guanine (CAG) trinucleotide repeat expansion (>48) in ATN1 gene at 12p13.31 locus inherited in an autosomal-dominant manner.
Pooja Sharma, Raja G Shaikh, Uzma Shamim, Vaishakh Anand, Biswaroop Chakrabarty, Sheffali Gulati, Akhilesh K Sonakar, Istaq Ahmad, Ajay Garg, Achal K Srivastava, Mohammed Faruq   +10 more
doaj   +1 more source

Altered Auditory Maturation in Fragile X Syndrome and Its Involvement in Audiogenic Seizure Susceptibility

Autism Research, Volume 19, Issue 1, January 2026.
ABSTRACT Auditory hypersensitivity is a prominent symptom in Fragile X syndrome (FXS), the most prevalent monogenic cause of autism and intellectual disability. FXS arises through the loss of the protein encoded by the FMR1 (Fragile X Messenger Ribonucleoprotein 1) gene, FMRP, required for normal neural circuit excitability.
Dorit Möhrle, Demi Ma, Wenyue Xue, Jun Yan, Ning Cheng   +4 more
wiley   +1 more source

The central role of DNA damage and repair in CAG repeat diseases

Disease Models & Mechanisms, 2018
Diseases such as Huntington's disease and certain spinocerebellar ataxias are caused by the expansion of genomic cytosine-adenine-guanine (CAG) trinucleotide repeats beyond a specific threshold.
Thomas H. Massey, Lesley Jones
doaj   +1 more source

Cerebellum-enriched protein INPP5A contributes to selective neuropathology in mouse model of spinocerebellar ataxias type 17

Nature Communications, 2020
It is not yet clear how ubiquitously-expressed proteins can cause the selective degeneration of particular populations of neurons, such as in spinocerebellar ataxia type 17, SCA17, which results from a CAG trinucleotide repeat expansion in the ...
Qiong Liu, Shanshan Huang, Peng Yin, Su Yang, Jennifer Zhang, Liang Jing, Siying Cheng, Beisha Tang, Xiao-Jiang Li, Yongcheng Pan, Shihua Li   +10 more
doaj   +1 more source

Contracting CAG/CTG repeats using the CRISPR-Cas9 nickase [PDF]

, 2016
CAG/CTG repeat expansions cause over 13 neurological diseases that remain without a cure. Because longer tracts cause more severe phenotypes, contracting them may provide a therapeutic avenue.
Aeschbach, Lorène, Cinesi, Cinzia, Dion, Vincent, Yang, Bin   +3 more
core   +3 more sources