Results 141 to 150 of about 340,510 (279)
Our study reveals the protective role of GPR124 in maintaining BBB integrity and promoting neurological recovery following TBI. It makes a significant contribution by uncovering a novel molecular interaction between GPR124 and FGFBP1 and linking this to activation of the Wnt/β‐catenin signaling pathway in vascular repair mechanisms.
Chen Wang +13 more
wiley +1 more source
Electroacupuncture (EA) ameliorates learning and memory function in 5×FAD mice by regulating the brain glucose metabolic network. This neuroprotective effect is closely related to enhancing neuronal energy utilization via the IGF1/IGF1R signaling pathway.
Shengxiang Liang +12 more
wiley +1 more source
Therapeutic approach for Alzheimer's Disease
The thesis main focus is on brief introduction, bit of history of Alzheimer's disease, the main theories that contribute to the disease development and the final is treatment options.
Wazir, Najib
core
Zinc Exposure Causes Disulfidptosis to Induce Miscarriage by Up‐Regulating GATA1/METTL1/SLC7A11 Axis
Zn exposure up‐regulates GATA1, promoting GATA1‐mediated METTL1 and SLC7A11 transcription. It also enhances METTL1‐mediated m7G modification on SLC7A11 mRNA, increasing SLC7A11 mRNA stability. Ultimately, Zn exposure up‐regulates SLC7A11 at both transcriptional and post‐transcriptional levels, causing disulfidptosis. Knockdown of murine Slc7a11, Gata1,
Wenxin Huang +16 more
wiley +1 more source
Cytoplasmic aggregation of TDP‐43 is a common pathological feature in amyotrophic lateral sclerosis, frontotemporal lobar degeneration, and Alzheimer's disease with TDP‐43 pathology. This study reports that wild‐type PDI slows down phase separation of TDP‐43 through direct interaction with TDP‐43.
Jia‐Qi Liu +14 more
wiley +1 more source
Alzheimer's disease and pharmacological treatments
The defect observed in adults with Alzheimer's disease is likely as a result of a complex interaction of biochemical interactions that ultimately cause neuronal damage.ultimately,our ability for the management of AD depends on having a correct view of ...
Davoodi, Neda
core
Neuronal PKM2‐driven glycolysis generates excess lactate that triggers histone H3K18 lactylation (H3K18la), establishing a pathogenic metabolic‐epigenetic axis in epilepsy. Elevated H3K18la enriches the Cop1 promoter, transcriptionally upregulating the E3 ubiquitin ligase COP1, which subsequently drives proteasomal degradation of GABAARβ2 and impairs ...
Yuan Meng +8 more
wiley +1 more source

