Results 81 to 90 of about 2,689,802 (421)

Critical appraisal on mitochondrial dysfunction in Alzheimer’s disease

AGING MEDICINE, Volume 5, Issue 4, Page 272-280, December 2022., 2022
Amyloid plaques deposit on neurons in case of Alzheimer's Disease. Mitochondria play a vital role in pathogenesis of Alzheimer's Disease. Mitochondrial dysfunction can lead to formation of mPTP, alteration of complexes 1,3 and 4, deficits in bioenergetics with impaired mitochondrial biogenesis. Abstract It is widely recognized that Alzheimer's disease (
Faizan Ahmad, Punya Sachdeva
wiley   +1 more source

Removal of AMPA receptors (AMPARs) from synapses is preceded by transient endocytosis of extrasynaptic AMPARs [PDF]

, 2004
AMPA receptors (AMPARs) are dynamically regulated at synapses, but the time course and location of their exocytosis and endocytosis are not known. Therefore, we have used ecliptic pHluorin-tagged glutamate receptor 2 to visualize changes in AMPAR surface
Ashby, MC, Collingridge, Graham L, De La Rue, Sarah A, Henley, Jeremy, Ralph, GS, Uney, James   +5 more
core   +1 more source

Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss

Proceedings of the National Academy of Sciences of the United States of America, 2013
Significance Communication between nerve cells occurs at specialized cellular structures known as synapses. Loss of synaptic function is associated with cognitive decline in Alzheimer’s disease (AD).
M. Talantova, Sara Sanz‐Blasco, Xiaofei Zhang, Peng Xia, M. W. Akhtar, S. Okamoto, G. Dziewczapolski, Tomohiro Nakamura, G. Cao, Alexander E Pratt, Yeon-Joo Kang, Shichun Tu, E. Molokanova, S. Mckercher, S. Hires, Hagit Sason, D. Stouffer, Matthew W Buczynski, James P. Solomon, Sarah Michael, E. Powers, J. Kelly, Amanda Roberts, Gary G Tong, Traci Fang-Newmeyer, James Parker, Emily A. Holland, Dongxian Zhang, N. Nakanishi, H. Chen, Herman Wolosker, Yuqiang Wang, L. Parsons, R. Ambasudhan, E. Masliah, S. Heinemann, J. Piña-Crespo, S. Lipton   +37 more
semanticscholar   +1 more source

Respiratory complex I‐mediated NAD+ regeneration regulates cancer cell proliferation through the transcriptional and translational control of p21Cip1 expression by SIRT3 and SIRT7

Molecular Oncology, EarlyView.
NAD+ regeneration by mitochondrial complex I NADH dehydrogenase is important for cancer cell proliferation. Specifically, NAD+ is necessary for the activities of NAD+‐dependent deacetylases SIRT3 and SIRT7, which suppress the expression of p21Cip1 cyclin‐dependent kinase inhibitor, an antiproliferative molecule, at the translational and transcriptional
Masato Higurashi, Kazunori Mori, Hidetsugu Nakagawa, Momoko Uchida, Fumihiro Ishikawa, Motoko Shibanuma   +5 more
wiley   +1 more source

Glutamate signaling through the NMDA receptor reduces the expression of scleraxis in plantaris tendon derived cells

BMC Musculoskeletal Disorders, 2017
Background A body of evidence demonstrating changes to the glutaminergic system in tendinopathy has recently emerged. This hypothesis was further tested by studying the effects of glutamate on the tenocyte phenotype, and the impact of loading and ...
Christoph Spang, Ludvig J. Backman, Sandrine Le Roux, Jialin Chen, Patrik Danielson   +4 more
doaj   +1 more source

A biophysical network model reveals the link between deficient inhibitory cognitive control and major neurotransmitter and neural connectivity hypotheses in schizophrenia [PDF]

arXiv, 2021
We address a biophysical network dynamical model to study how the modulation of dopamine (DA) activity and related N-methyl-d-aspartate (NMDA) glutamate receptor activity as well as the emerging Pre-Frontal Cortex (PFC) functional connectivity network (FCN) affect inhibitory cognitive function in schizophrenia in an antisaccade task.
arxiv  

Uncoupling of the endocannabinoid signalling complex in a mouse model of fragile X syndrome [PDF]

, 2012
Fragile X syndrome, the most commonly known genetic cause of autism, is due to loss of the fragile X mental retardation protein, which regulates signal transduction at metabotropic glutamate receptor-5 in the brain.
DiPatrizio, Nicholas V., Frick, Andreas, Ginger, Melanie, Henstridge, Christopher M., Jung, Kwang-Mook, Katona, Istvan, Lassalle, Olivier, Mackie, Ken, Manzoni, Olivier J., Martin, Henry, Neuhofer, Daniela, Piomelli, Daniele, Sepers, Marja   +12 more
core   +5 more sources

Glutamate Receptors: Desensitizing Dimers [PDF]

Current Biology, 2002
Recent structural studies show, not only how the desensitization of a ligand-gated ion channel with bound agonist can be rationalized in terms of subunit-subunit instability, but also how a previously unknown mode of interaction may provide clues into how the receptor is tetramerically assembled in vivo.
openaire   +3 more sources

Escape from TGF‐β‐induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

Molecular Oncology, EarlyView.
Chronic TGF‐β exposure drives epithelial HCC cells from a senescent state to a TGF‐β resistant mesenchymal phenotype. This transition is characterized by the loss of Smad3‐mediated signaling, escape from senescence, enhanced invasiveness and metastatic potential, and upregulation of key resistance modulators such as MARK1 and GRM8, ultimately promoting
Minenur Kalyoncu, Dilara Demirci, Sude Eris, Bengisu Dayanc, Ece Cakiroglu, Merve Basol, Merve Uysal, Gulcin Cakan‐Akdogan, Fang Liu, Mehmet Ozturk, Gökhan Karakülah, Serif Senturk   +11 more
wiley   +1 more source

Retinal Glutamate Neurotransmission: From Physiology to Pathophysiological Mechanisms of Retinal Ganglion Cell Degeneration

Life, 2022
Glutamate neurotransmission and metabolism are finely modulated by the retinal network, where the efficient processing of visual information is shaped by the differential distribution and composition of glutamate receptors and transporters.
Isabella Boccuni, Richard Fairless
doaj   +1 more source