Results 81 to 90 of about 19,301 (220)

Galectin-3 aggravates microglial activation and tau transmission in tauopathy

The Journal of Clinical Investigation
Alzheimer’s disease is characterized by the accumulation of amyloid-β plaques, aggregation of hyperphosphorylated tau (pTau), and microglia activation.
Jian Jing Siew, Hui-Mei Chen, Feng-Lan Chiu, Chia-Wei Lee, Yao-Ming Chang, Hung-Lin Chen, Thi Ngoc Anh Nguyen, Hung-Ting Liao, Mengyu Liu, Hsiao-Tien Hagar, Yung-Chen Sun, Hsing-Lin Lai, Min-Hao Kuo, David Blum, Luc Buée, Lee-Way Jin, Shih-Yu Chen, Tai-Ming Ko, Jie-Rong Huang, Hung-Chih Kuo, Fu-Tong Liu, Yijuang Chern   +21 more
doaj   +1 more source

Stimulating proteasomal degradation in human proteinopathies

The FEBS Journal, EarlyView.
The proteasome mediates the degradation of a wide range of proteins. Boosting proteasomal degradation may be beneficial in several disease contexts and can be achieved either by modulating proteasome activity or by improving substrate delivery. Proteasome activity can be enhanced by increasing proteasome abundance, inducing constitutive gate opening ...
Maria E. Gierisch, Enrica Barchi, Nico P. Dantuma   +2 more
wiley   +1 more source

Young Adult Microglial Deletion of C1q Reduces Engulfment of Synapses and Partially Mitigates Cognitive Impairment in an Aggressive Alzheimer's Disease Mouse Model

Glia, Volume 74, Issue 9, September 2026.
Young adult deletion of microglial C1q reduced engulfment of Vglut1+ synapses and mitigated spatial cognitive deficits at 10 months of age in the amyloidopathy Arctic mouse model of AD. Neither fibrillar amyloid plaques nor soluble or insoluble Aβ levels in the hippocampus were affected by young adult microglial loss of C1q despite reduced phagocytosis
Tiffany J. Petrisko, Shu‐Hui Chu, Angela Gomez‐Arboledas, Blossom Zhang, Andrea J. Tenner   +4 more
wiley   +1 more source

Discovery and characterization of stereodefined PMO-gapmers targeting tau

Molecular Therapy: Nucleic Acids
Antisense oligonucleotides (ASOs) are an important class of therapeutics to treat genetic diseases, and expansion of this modality to neurodegenerative disorders has been an active area of research.
Kunihiko Kanatsu, Yoshinori Takahashi, Tetsuya Sakaguchi, Dae-Shik Kim, Miki Murota, Mingde Shan, Kazuki Fukami, Wataru Itano, Kenji Kikuta, Hikaru Yoshimura, Toshiki Kurokawa, Yuko Nagayama, Rena Ishikawa, Ryo Dairiki, Zhi Zhou, Kristen Sanders, Jacob Stupalski, So Yasui, Diana Liu, Farid Benayoud, Hui Fang, Enxuan Jing, Makoto Ogo, Francis G. Fang, John Wang, Hyeong-wook Choi   +25 more
doaj   +1 more source

Elevated Plasma Phospho‐Tau217 in Beta‐Propeller Protein‐Associated Neurodegeneration

Movement Disorders, EarlyView.
Jae‐Hyeok Lee, Yun Soo Kim
wiley   +1 more source

Fisetin Attenuates Amyloid‐Beta‐Induced Neurotoxicity in Human Neuroblastoma SH‐SY5Y Cells: Integrating In Silico Target Prediction and In Vitro Validation

Journal of Biochemical and Molecular Toxicology, Volume 40, Issue 9, September 2026.
The in‐silico data showed that fisetin binds stably with the autophagy receptors and synaptic density regulators. Further, in‐vitro data confirmed the restoration of Aβ1‐42 disrupted autophagy by fisetin. Fisetin restored the oxidative stress and ion channels, along with a reduction of AChE activity.
Charu Jaiswal, Ishika Singh, Abhishek Kumar Singh   +2 more
wiley   +1 more source

A Mathematical Model of Cellular Aggregation Predicts Patterns of Tau Accumulation in Neurodegenerative Disease

Advanced Science
Protein aggregates are a hallmark of neurodegenerative disease, yet the molecular processes that control their appearance remain incompletely characterized.
Shih‐Huan Huang, Annelies Quaegebeur, Tanrada Pansuwan, Timothy Rittman, Ruiyan Wang, Tuomas PJ Knowles, James B Rowe, David Klenerman, Georg Meisl   +8 more
doaj   +1 more source

Cell Death in Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Targets

MedComm, Volume 7, Issue 9, September 2026.
Regulated cell death pathways, including apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy‐dependent cell death, interact with mitochondrial dysfunction, proteostasis failure, lysosomal stress, glial remodeling, and neuroinflammation across major neurodegenerative diseases.
Tianjiao Li, Qian Zhang, Yichen Wu, Ruixue Huang   +3 more
wiley   +1 more source

Increased expression of inflammasome signaling genes and proteins in selective brain regions in the intermediate stage of Alzheimer's disease

Brain Pathology, Volume 36, Issue 5, September 2026.
Neuritic plaques increase in the intermediate stage of Alzheimer's neuropathological change. The intermediate stage of Alzheimer's disease was investigated by transcriptomics and immunohistochemistry. This revealed that inflammasome sensors NLRP1, NLRP3, and AIM2 oligomerize with ASC speck to form the inflammasome complex and initiate the downstream ...
Juan Pablo de Rivero Vaccari, David A. Davis, Andrew P. Sawaya, Susanna P. Garamszegi, Xiaoyan Sun, Ayled Barreda, Helen M. Bramlett, Sakir Humayun Gultekin, W. Dalton Dietrich, Robert W. Keane, Regina T. Vontell   +10 more
wiley   +1 more source

Progression to Dementia in Very Late‐Onset Schizophrenia‐Like Psychosis Stratified by Alzheimer's Disease and Lewy Body Disease Biomarkers: A Retrospective Cohort Study

Psychogeriatrics, Volume 26, Issue 5, September 2026.
ABSTRACT Background Very late‐onset schizophrenia‐like psychosis (VLOSLP) is clinically heterogeneous, and its relationship with dementia‐related neurodegenerative disease remains unresolved. We examined whether Alzheimer's disease (AD) and Lewy body disease (LBD) biomarker status were associated with dementia progression in VLOSLP.
Yuto Satake, Hideki Kanemoto, Daiki Taomoto, Kayo Takeda, Shigeki Katakami, Matasaburo Kobayashi, Keiko Matsunaga, Kayako Isohashi, Takashi Suehiro, Kenji Yoshiyama, Manabu Ikeda   +10 more
wiley   +1 more source