| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Paul D Coleman, Elaine Delvaux, Jeffrey H Kordower, Ashley Boehringer, Carol J Huseb. Massive changes in gene expression and their cause(s) can be a unifying principle in the pathobiology of Alzheimer's disease. Alzheimer's & dementia : the journal of the Alzheimer's Association. 2025-02-06. PMID:39912452. |
understanding of the biology of alzheimer's disease (ad) has long been fragmented, with various investigators concentrating on amyloid beta (aβ) or tau, inflammation, cell death pathways, misfolded proteins, glia, and more. |
2025-02-06 |
2025-02-08 |
Not clear |
| Jinwang Ye, Suyue Zhong, Huali Wan, Xing Guo, Xuanbao Yao, Qiong Liu, Liming Chen, Jian-Zhi Wang, Shifeng Xia. Upregulated astrocyte HDAC7 induces Alzheimer-like tau pathologies via deacetylating transcription factor-EB and inhibiting lysosome biogenesis. Molecular neurodegeneration. vol 20. issue 1. 2025-01-14. PMID:39806423. |
astrocytes, the most abundant glial cell type in the brain, will convert into the reactive state in response to proteotoxic stress such as tau accumulation, a characteristic feature of alzheimer's disease (ad) and other tauopathies. |
2025-01-14 |
2025-01-31 |
Not clear |
| Sheina Emrani, Sanaz Arezoumandan, Katheryn A Q Cousins, Noah Capp, Eddie B Lee, David A Wolk, Paul A Yushkevich, Corey T McMillan, M Dylan Tisdall, David J Irwi. Basic Science and Pathogenesis. Alzheimer's & dementia : the journal of the Alzheimer's Association. vol 20 Suppl 1. 2025-01-03. PMID:39750861. |
we hypothesize neuroinflammation marked by flc-reactive glia may relate to protein aggregation and contribute to partially distinct regional patterns of tau vs tdp-43 propagation in ftld. |
2025-01-03 |
2025-01-05 |
Not clear |
| Grace A Selecky, Kristen R Whitney, Margaret M Krassner, Alessandra Cervera, Claudia De Sanctis, Victoria Flores Almazan, Sean Thomas Delica, SoongHo Kim, Kurt W Farrell, Thomas D Christie, Megan A Iida, Lily Sarrafha, Gustavo Parfitt, Ruth H Walker, Melissa J Nirenberg, Giulietta M Riboldi, Steven J Frucht, Tim Ahfeldt, Sally Temple, John F Crar. Basic Science and Pathogenesis. Alzheimer's & dementia : the journal of the Alzheimer's Association. vol 20 Suppl 1. 2025-01-03. PMID:39751331. |
the accumulation of abnormal tau protein in neurons and glia in the human brain is the defining feature of neurodegenerative diseases known as tauopathies. |
2025-01-03 |
2025-01-05 |
human |
| Xia Han, Jessica E Rexac. Basic Science and Pathogenesis. Alzheimer's & dementia : the journal of the Alzheimer's Association. vol 20 Suppl 1. 2025-01-03. PMID:39751501. |
abnormal tau protein accumulation selectively affects distinct brain regions and specific neuron and glia populations in tau-related dementias like alzheimer's disease (ad), frontotemporal dementia (ftd, pick's disease type), and progressive supranuclear palsy (psp). |
2025-01-03 |
2025-01-05 |
Not clear |
| Kristen Whitney, Won-Min Song, Abhijeet Sharma, Diana K Dangoor, Kurt Farrell, Margaret M Krassner, Hadley W Ressler, Thomas D Christie, Shrishtee Kandoi, Ruth H Walker, Melissa J Nirenberg, Steven J Frucht, Giulietta M Riboldi, Bin Zhang, Ana C Pereira, John F Crar. Single-cell transcriptomic and neuropathologic analysis reveals dysregulation of the integrated stress response in progressive supranuclear palsy. Acta neuropathologica. vol 148. issue 1. 2024-12-08. PMID:39648200. |
progressive supranuclear palsy (psp) is a sporadic neurodegenerative tauopathy variably affecting brainstem and cortical structures, and characterized by tau inclusions in neurons and glia. |
2024-12-08 |
2024-12-11 |
human |
| C Alexander Sandhof, Heide F B Murray, M Catarina Silva, Stephen J Haggart. Targeted protein degradation with bifunctional molecules as a novel therapeutic modality for Alzheimer's disease & beyond. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics. 2024-12-05. PMID:39638711. |
the events leading to neuronal death are associated with the accumulation of aggregating proteins in neurons and glia of the affected brain regions, in particular extracellular deposition of amyloid plaques and intracellular formation of tau neurofibrillary tangles. |
2024-12-05 |
2024-12-08 |
Not clear |
| Yuen-Shan Ho, Wai-Yin Cheng, Michael Siu-Lun Lai, Chi-Fai Lau, Gordon Tin-Chun Wong, Wing-Fai Yeung, Raymond Chuen-Chung Chan. Postoperative Electroacupuncture Boosts Cognitive Function Recovery after Laparotomy in Mice. Biomolecules. vol 14. issue 10. 2024-10-26. PMID:39456207. |
ea also reduced tau phosphorylation and suppressed the activation of tau-related kinases and glia, with effects comparable to ibuprofen. |
2024-10-26 |
2024-10-29 |
mouse |
| Xuetao Qi, Shulu Yuan, Jiuyang Ding, Weiqi Sun, Yajiao Shi, Yuanwei Xing, Zilong Liu, Yun Yao, Su Fu, Baofei Sun, Xiaolan Qi, Bing Xia, Fengyu Liu, Ming Yi, Jian Mao, You Wan, Jie Zhen. Emerging signs of Alzheimer-like tau hyperphosphorylation and neuroinflammation in the brain post recovery from COVID-19. Aging cell. 2024-09-30. PMID:39344133. |
here, using postmortem human brain samples, we found abnormal accumulation of hyperphosphorylated tau protein in the hippocampus and medial entorhinal cortex within 4-13 months post clinically recovery from acute covid-19, together with prolonged activation of glia cells and increases in inflammatory factors, even though no sars-cov-2 invasion was detected in these regions. |
2024-09-30 |
2024-10-02 |
human |
| Mia R Burke, Ioannis Sotiropoulos, Clarissa L Waite. The multiple roles of chronic stress and glucocorticoids in Alzheimer's disease pathogenesis. Trends in neurosciences. 2024-09-22. PMID:39307629. |
we specifically discuss the effects of chronic stress and gcs on tau pathogenesis, including hyperphosphorylation, aggregation, and spreading, amyloid precursor protein (app) processing and trafficking culminating in aβ production, immune priming by proinflammatory cytokines and disease-associated molecular patterns, and alterations to glial cell and blood-brain barrier (bbb) function. |
2024-09-22 |
2024-09-26 |
Not clear |
| Kurt Farrell, Jack Humphrey, Timothy Chang, Yi Zhao, Yuk Yee Leung, Pavel P Kuksa, Vishakha Patil, Wan-Ping Lee, Amanda B Kuzma, Otto Valladares, Laura B Cantwell, Hui Wang, Ashvin Ravi, Claudia De Sanctis, Natalia Han, Thomas D Christie, Robina Afzal, Shrishtee Kandoi, Kristen Whitney, Margaret M Krassner, Hadley Ressler, SoongHo Kim, Diana Dangoor, Megan A Iida, Alicia Casella, Ruth H Walker, Melissa J Nirenberg, Alan E Renton, Bergan Babrowicz, Giovanni Coppola, Towfique Raj, Günter U Höglinger, Ulrich Müller, Lawrence I Golbe, Huw R Morris, John Hardy, Tamas Revesz, Tom T Warner, Zane Jaunmuktane, Kin Y Mok, Rosa Rademakers, Dennis W Dickson, Owen A Ross, Li-San Wang, Alison Goate, Gerard Schellenberg, Daniel H Geschwind, John F Crary, Adam Na. Genetic, transcriptomic, histological, and biochemical analysis of progressive supranuclear palsy implicates glial activation and novel risk genes. Nature communications. vol 15. issue 1. 2024-09-09. PMID:39251599. |
psp differs from alzheimer's disease (ad) and other diseases, displaying abnormal microtubule-associated protein tau by both neuronal and glial cell pathologies. |
2024-09-09 |
2024-09-13 |
Not clear |
| L Daniel Estrella, Jane E Manganaro, Lexi Sheldon, Nashanthea Roland, Austin D Snyder, Joseph W George, Katy Emanuel, Benjamin G Lamberty, Kelly L Stauc. Chronic glial activation and behavioral alterations induced by acute/subacute pioglitazone treatment in a mouse model of traumatic brain injury. Brain, behavior, and immunity. 2024-09-06. PMID:39242055. |
acute/subacute pioglitazone treatment after tbi results in long-term deleterious consequences, including disruption of tau homeostasis, chronic glial cell activation, neuronal pathology, and worsened injury severity particularly at 274 dpi, with male mice being more susceptible than female mice. |
2024-09-06 |
2024-09-10 |
mouse |
| Lindsey D Goodman, Isha Ralhan, Xin Li, Shenzhao Lu, Matthew J Moulton, Ye-Jin Park, Pinghan Zhao, Oguz Kanca, Ziyaneh S Ghaderpour Taleghani, Julie Jacquemyn, Joshua M Shulman, Kanae Ando, Kai Sun, Maria S Ioannou, Hugo J Belle. Tau is required for glial lipid droplet formation and resistance to neuronal oxidative stress. Nature neuroscience. 2024-08-26. PMID:39187706. |
the accumulation of reactive oxygen species (ros) is a common feature of tauopathies, defined by tau accumulations in neurons and glia. |
2024-08-26 |
2024-08-30 |
human |
| Lindsey D Goodman, Isha Ralhan, Xin Li, Shenzhao Lu, Matthew J Moulton, Ye-Jin Park, Pinghan Zhao, Oguz Kanca, Ziyaneh S Ghaderpour Taleghani, Julie Jacquemyn, Joshua M Shulman, Kanae Ando, Kai Sun, Maria S Ioannou, Hugo J Belle. Tau is required for glial lipid droplet formation and resistance to neuronal oxidative stress. Nature neuroscience. 2024-08-26. PMID:39187706. |
we found that overexpressing tau in glia disrupts lds in flies and rat neuron-astrocyte co-cultures, sensitizing the glia to toxic, neuronal lpos. |
2024-08-26 |
2024-08-30 |
human |
| Lindsey D Goodman, Isha Ralhan, Xin Li, Shenzhao Lu, Matthew J Moulton, Ye-Jin Park, Pinghan Zhao, Oguz Kanca, Ziyaneh S Ghaderpour Taleghani, Julie Jacquemyn, Joshua M Shulman, Kanae Ando, Kai Sun, Maria S Ioannou, Hugo J Belle. Tau is required for glial lipid droplet formation and resistance to neuronal oxidative stress. Nature neuroscience. 2024-08-26. PMID:39187706. |
overall, this work provides insights into the important role that tau has in glia to mitigate ros in the brain. |
2024-08-26 |
2024-08-30 |
human |
| Samantha R Pierson, Kimberly L Fiock, Ruixiang Wang, Nagalakshmi Balasubramanian, Jessica Reinhardt, Kanza M Khan, Thomas D James, Mikayla L Hunter, Benjamin J Cooper, Hannah R Williamsen, Ryan Betters, Kaancan Deniz, Gloria Lee, Georgina Aldridge, Marco M Hefti, Catherine A Marcinkiewc. Tau pathology in the dorsal raphe may be a prodromal indicator of Alzheimer's disease. Molecular psychiatry. 2024-08-14. PMID:39143322. |
tau pathology was predominantly found in neurons relative to glia and colocalized with a significant proportion of tph2-expressing neurons in the drn. |
2024-08-14 |
2024-08-17 |
mouse |
| Qiusha Li, Han Liu, Qingyong Zhu, Rui Zhang, Dongxiao Liang, Jingwen Zhang, Ruoqi Jin, Yongkang Chen, Chi Qin, Junfang Ten. Induction of tau pathology and motor dysfunction in mice by urinary exosomes from progressive supranuclear palsy patients. Brain research bulletin. 2024-08-07. PMID:39111605. |
progressive supranuclear palsy (psp) is characterized by the presence of hyperphosphorylated and misfolded tau aggregates in neurons and glia. |
2024-08-07 |
2024-08-10 |
mouse |
| Yunfan Long, Jiajia Liu, Yu Wang, Haidong Guo, Guohong Cu. The complex effects of miR-146a in the pathogenesis of Alzheimer's disease. Neural regeneration research. vol 20. issue 5. 2024-07-30. PMID:39075895. |
we aim to elucidate the relationship between mir-146a and the key pathological manifestations of alzheimer's disease, such as amyloid-β deposition, tau protein hyperphosphorylation, neuronal death, mitochondrial dysfunction, synaptic dysfunction, and glial cell dysfunction, as well as summarize recent relevant studies that have highlighted the potential of mir-146a as a clinical diagnostic marker and therapeutic target for alzheimer's disease. |
2024-07-30 |
2024-08-02 |
Not clear |
| Melinda L Johnson, Mechelle M Lewis, Ernest W Wang, Leslie C Jellen, Guangwei Du, Sol De Jesus, Lan Kong, Cunfeng Pu, Xuemei Huan. Neuropathological findings and in vivo imaging correlates of the red nucleus compared to those of the substantia nigra pars compacta in parkinsonisms. Parkinsonism & related disorders. vol 125. 2024-06-19. PMID:38896976. |
recently, in vivo susceptibility mri metrics were associated with postmortem glial cell density and tau burden in the snc of parkinsonism subjects. |
2024-06-19 |
2024-06-22 |
human |
| Madia Lozupone, Vittorio Dibello, Antonio Daniele, Vincenzo Solfrizzi, Emanuela Resta, Francesco Panz. How can we manage progressive supranuclear palsy syndrome with pharmacotherapy? Expert opinion on pharmacotherapy. 2024-04-23. PMID:38653731. |
tauopathies are a spectrum of clinicopathological neurodegenerative disorders with increased aggregates included in glia and/or neurons of hyperphosphorylated insoluble tau protein, a microtubule-associated protein. |
2024-04-23 |
2024-04-26 |
Not clear |