All Relations between microtubule-associated protein tau and cerebral cortex

Publication Sentence Publish Date Extraction Date Species
C Leonardo Jimenez Chavez, Gavin P Scheldrup, Lauren E Madory, Christopher J E Denning, Edward C Lee, Dylan T Nguyen, Marian Castro, Andrew Garcia, Jose Torres-Gonzales, Jessica N Herbert, Daniel Kotlyar, Neda Riazat, William Pakter, William Le, Eliyanna Van Doren, Marianna Ter Galstian, Karen K Szumlinsk. Biochemical changes precede affective and cognitive anomalies in aging adult C57BL/6J mice with a prior history of adolescent alcohol binge-drinking. Addiction biology. vol 29. issue 12. 2024-12-12. PMID:39665499. behavioural testing was then followed by immunoblotting to index the protein expression of glutamate receptors, neuropathological markers [tau, p (thr217)-tau, p (ser396)-tau, bace, app, aβ], as well as erk activation within the entorhinal cortex, prefrontal cortex and amygdala. 2024-12-12 2024-12-14 mouse
Noha Aladdin, Salah A Gharei. Vitamin D3 Exerts a Neuroprotective Effect in Metabolic Syndrome Rats: Role of BDNF/TRKB/Akt/GS3Kβ Pathway. Journal of biochemical and molecular toxicology. vol 38. issue 12. 2024-12-09. PMID:39651608. the advanced glycation end products (ages), and markers of inflammation (tnf-α and nf-κb), oxidative stress (malondialdehyde), and apoptosis (caspase3), as well as bdnf, trkb, pi3k, akt, gsk3β, phosphorylated tau, and amyloid beta (aβ) were assessed in the cerebral cortex. 2024-12-09 2024-12-12 rat
Jacob Ziontz, Theresa M Harrison, Corrina Fonseca, Joseph Giorgio, Feng Han, JiaQie Lee, William J Jagus. Connectivity, Pathology, and ApoE4 Interactions Predict Longitudinal Tau Spatial Progression and Memory. Human brain mapping. vol 45. issue 17. 2024-12-09. PMID:39651679. connectivity between tau epicenters and later accumulating regions of cortex has been proposed as a mechanism of tau spread, but how this relationship changes with greater ad pathology burden or genotype is not understood. 2024-12-09 2024-12-12 Not clear
Kaitlyn M Dybing, Cecelia J Vetter, Desarae A Dempsey, Soumilee Chaudhuri, Andrew J Saykin, Shannon L Risache. Traumatic Brain Injury and Alzheimer's Disease Biomarkers: A Systematic Review of Findings from Amyloid and Tau Positron Emission Tomography. Journal of neurotrauma. 2024-12-06. PMID:39639808. evidence for elevated tau was strongest in the medial temporal lobe, entorhinal cortex, precuneus, and frontal, temporal, parietal, and occipital lobes. 2024-12-06 2024-12-08 Not clear
Vanessa Alexandre-Silva, Beatriz Soares-Silva, Gabrielle Christine Pereira, Ana Claúdia Custódio-Silva, Patrícia Santos Carvalhinho-Lopes, Luciana Oliveira Taliano, Rafael Herling Lambertucci, Marcelo Duarte Cavalcante, Adriano Antunes de Souza Araújo, Lucindo Quintans-Júnior, José Ronaldo Dos Santos, Alessandra Mussi Ribeir. Eplingiella fruticosa leaf essential oil complexed with β-cyclodextrin exerts a neuroprotective effect in an Alzheimer's disease animal model induced by Streptozotocin. Metabolic brain disease. vol 40. issue 1. 2024-11-23. PMID:39579243. stz-treated rats showed memory deficits and anhedonia, accompanied by increased aβ, tau, and il-1β immunoreactivity in the olfactory bulb, cortex, hippocampus, and increased tbars levels in the hippocampus. 2024-11-23 2024-11-26 rat
Vanessa Alexandre-Silva, Beatriz Soares-Silva, Gabrielle Christine Pereira, Ana Claúdia Custódio-Silva, Patrícia Santos Carvalhinho-Lopes, Luciana Oliveira Taliano, Rafael Herling Lambertucci, Marcelo Duarte Cavalcante, Adriano Antunes de Souza Araújo, Lucindo Quintans-Júnior, José Ronaldo Dos Santos, Alessandra Mussi Ribeir. Eplingiella fruticosa leaf essential oil complexed with β-cyclodextrin exerts a neuroprotective effect in an Alzheimer's disease animal model induced by Streptozotocin. Metabolic brain disease. vol 40. issue 1. 2024-11-23. PMID:39579243. additionally, ef treatment decreased aβ, tau, and il-1β immunoreactivity in the olfactory bulb, hippocampus and cortex (p < 0.05), and reduced tbars levels (p = 0.04) and total oxidant status in the hippocampus (p = 0.03), and increased total antioxidant status in the cortex (p = 0.04). 2024-11-23 2024-11-26 rat
Stanislau Hrybouski, Sandhitsu R Das, Long Xie, Christopher A Brown, Melissa Flamporis, Jacqueline Lane, Ilya M Nasrallah, John A Detre, Paul A Yushkevich, David A Wol. BOLD Amplitude Correlates of Preclinical Alzheimer's Disease. medRxiv : the preprint server for health sciences. 2024-11-22. PMID:39574853. in preclinical ad, amyloid positivity was associated with a spatially diffuse alff reduction in the frontal, medial parietal, and lateral temporal association cortices, while tau pathology was negatively associated with alff in the entorhinal cortex. 2024-11-22 2024-11-24 Not clear
Marisa Denkinger, Suzanne Baker, Theresa M Harrison, Trevor Chadwick, William J Jagus. Cross-sectional and longitudinal relationships among blood-brain barrier disruption, Alzheimer's disease biomarkers, and cognition in cognitively normal older adults. Neurobiology of aging. vol 146. 2024-11-21. PMID:39571410. in participants with longitudinal ad biomarker and cognitive data acquired prior to dce-mri, faster longitudinal entorhinal cortex (ec) tau accumulation and episodic memory decline were associated with greater hc bbbd, independent of global aβ changes and regional atrophy. 2024-11-21 2024-11-24 human
KeShangJing Wu, QingSong Liu, KeYu Long, XueQing Duan, XianYu Chen, Jing Zhang, Li Li, Bin L. Deciphering the role of lipid metabolism-related genes in Alzheimer's disease: a machine learning approach integrating Traditional Chinese Medicine. Frontiers in endocrinology. vol 15. 2024-11-07. PMID:39507054. alzheimer's disease (ad) represents a progressive neurodegenerative disorder characterized by the accumulation of misfolded amyloid beta protein, leading to the formation of amyloid plaques and the aggregation of tau protein into neurofibrillary tangles within the cerebral cortex. 2024-11-07 2024-11-09 Not clear
Christopher Armstrong, Dan Luo, Anna Gretzinger, Deepti Pandey, Andrew Lipchik, Sokol V Todi, Aloke K Dutt. Novel Piperazine Based Compounds Target Alzheimer's Disease Relevant Amyloid β42 and Tau Derived Peptide AcPHF6, and the Lead Molecule Increases Viability in the Flies Expressing Human Tau Protein. ACS chemical neuroscience. vol 15. issue 21. 2024-11-06. PMID:39501783. the aggregation of amyloid β (senile plaques) and tau tangles (nfts) results in the death of neurons in the cortex and hippocampus, which manifests itself in cognitive decline and memory loss. 2024-11-06 2024-11-08 human
Simi Zhang, Chelsea Ann Crossley, Qi Yua. Neuronal Vulnerability of the Entorhinal Cortex to Tau Pathology in Alzheimer's Disease. British journal of biomedical science. vol 81. 2024-10-22. PMID:39435008. neuronal vulnerability of the entorhinal cortex to tau pathology in alzheimer's disease. 2024-10-22 2024-10-24 Not clear
Simi Zhang, Chelsea Ann Crossley, Qi Yua. Neuronal Vulnerability of the Entorhinal Cortex to Tau Pathology in Alzheimer's Disease. British journal of biomedical science. vol 81. 2024-10-22. PMID:39435008. this review delves into the entorhinal cortex (ec) as a central player in the pathogenesis of alzheimer's disease (ad), emphasizing its role in the accumulation and propagation of tau pathology. 2024-10-22 2024-10-24 Not clear
Yuta Katsumi, Inola A Howe, Ryan Eckbo, Bonnie Wong, Megan Quimby, Daisy Hochberg, Scott M McGinnis, Deepti Putcha, David A Wolk, Alexandra Touroutoglou, Bradford C Dickerso. Default mode network tau predicts future clinical decline in atypical early Alzheimer's disease. Brain : a journal of neurology. 2024-10-16. PMID:39412999. across heterogeneous clinical phenotypes, patients with atypical ad consistently exhibit abnormal tau accumulation in the posterior nodes of the default mode network of the cerebral cortex. 2024-10-16 2024-10-19 Not clear
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
Kelly Del Tredici, Michael Schön, Simone Feldengut, Estifanos Ghebremedhin, Sarah K Kaufman, Diana Wiesner, Francesco Roselli, Benjamin Mayer, Katrin Amunts, Heiko Braa. Early CA2 Tau Inclusions Do Not Distinguish an Age-Related Tauopathy from Early Alzheimer's Disease. Journal of Alzheimer's disease : JAD. 2024-09-20. PMID:39302368. recently, an early focus of tau inclusions in the ammon's horn second sector (ca2) with relative sparing of ca1 that occurs before tau inclusions develop in the entorhinal cortex (ec) was proposed as an additional feature of part. 2024-09-20 2024-09-22 Not clear
Senthilkumar Sivanesan, Matthew D Howell, Vibha Kaushik, Rajadas Jayakumar, Shree Mukilan Pari, Pankaj Goya. Multifunctional Tasks and an Energy Crisis are Crucial Players in Determining the Vulnerability of the Entorhinal Cortex to Early Damage in Alzheimer's Disease. Current Alzheimer research. 2024-09-16. PMID:39279693. it originates in the brain's entorhinal cortex (ec), with tau pathology that can proceed overt symptoms by decades and then spreads to other connected areas and networks to cause severe cognitive decline. 2024-09-16 2024-09-18 Not clear
Giuseppe D Ciccotosto, Ali I Mohammed, Rita Paolini, Elly Bijlsma, Su Toulson, James Holden, Eric C Reynolds, Stuart G Dashper, Catherine A Butle. Chronic Oral Inoculation of Porphyromonas gingivalis and Treponema denticola Induce Different Brain Pathologies in a Mouse Model of Alzheimer Disease. The Journal of infectious diseases. vol 230. issue Supplement_2. 2024-09-10. PMID:39255392. p. gingivalis alone significantly increased all 7 brain pathologies examined: neuronal damage, activation of astrocytes and microglia, expression of inflammatory cytokines interleukin 1β (il-1β) and interleukin 6 and production of amyloid-β plaques and hyperphosphorylated tau, in the hippocampus, cortex and midbrain, compared to control mice. 2024-09-10 2024-09-13 mouse
Giuseppe D Ciccotosto, Ali I Mohammed, Rita Paolini, Elly Bijlsma, Su Toulson, James Holden, Eric C Reynolds, Stuart G Dashper, Catherine A Butle. Chronic Oral Inoculation of Porphyromonas gingivalis and Treponema denticola Induce Different Brain Pathologies in a Mouse Model of Alzheimer Disease. The Journal of infectious diseases. vol 230. issue Supplement_2. 2024-09-10. PMID:39255392. coinoculation of p. gingivalis with t. denticola significantly increased activation of astrocytes and microglia in the hippocampus, cortex and midbrain, and increased production of hyperphosphorylated tau and il-1β in the hippocampus only. 2024-09-10 2024-09-13 mouse
Annie M Goettemoeller, Emmie Banks, Prateek Kumar, Viktor J Olah, Katharine E McCann, Kelly South, Christina C Ramelow, Anna Eaton, Duc M Duong, Nicholas T Seyfried, David Weinshenker, Srikant Rangaraju, Matthew J M Rowa. Entorhinal cortex vulnerability to human APP expression promotes hyperexcitability and tau pathology. Nature communications. vol 15. issue 1. 2024-09-10. PMID:39256379. entorhinal cortex vulnerability to human app expression promotes hyperexcitability and tau pathology. 2024-09-10 2024-09-13 mouse
Dario Bachmann, Antje Saake, Sandro Studer, Andreas Buchmann, Katrin Rauen, Esmeralda Gruber, Lars Michels, Roger M Nitsch, Christoph Hock, Anton Gietl, Valerie Treye. Hypertension and cerebral blood flow in the development of Alzheimer's disease. Alzheimer's & dementia : the journal of the Alzheimer's Association. 2024-09-10. PMID:39254220. we investigated the interactive associations between amyloid and hypertension on the entorhinal cortex (ec) tau and atrophy and the role of cerebral blood flow (cbf) as a shared mechanism by which amyloid and hypertension contribute to ec tau and regional white matter hyperintensities (wmhs). 2024-09-10 2024-09-13 Not clear