Results 111 to 120 of about 9,496,868 (341)

De-regulation of gene expression and alternative splicing affects distinct cellular pathways in the aging hippocampus

Frontiers in Cellular Neuroscience, 2014
Aging is accompanied by gradually increasing impairment of cognitive abilities and constitutes the main risk factor of neurodegenerative conditions like Alzheimer’s disease. The underlying mechanisms are however not well understood.
Roman M Stilling, Roman M Stilling, Eva eBenito, Michael eGertig, Vincenzo eCapece, Jonas eBarth, Susanne eBurkhardt, Stefan eBonn, Andre eFischer, Andre eFischer   +9 more
doaj   +1 more source

Genome-wide association study of behavioural and psychiatric features in human prion disease. [PDF]

, 2015
Prion diseases are rare neurodegenerative conditions causing highly variable clinical syndromes, which often include prominent neuropsychiatric symptoms.
Carswell, C, Collinge, J, Lowe, J, Lukic, A, MacKay, A, Mead, S, Porter, MC, Rudge, P, Thompson, AG, Uphill, J   +9 more
core   +1 more source

Downregulation of O‐GlcNAcylation enhances etoposide‐induced p53‐mediated apoptosis in HepG2 human liver cancer cells

FEBS Open Bio, EarlyView.
Etoposide, a topoisomerase II inhibitor, reduces O‐GlcNAcylation in HepG2 liver cancer cells. Further inhibition of O‐GlcNAc transferase by OSMI‐1 enhanced etoposide‐induced apoptosis, lowering the IC50 for viability and increasing the EC50 for cytotoxicity.
Jaehoon Lee, Gi‐Bang Koo, Jihye Park, Byung‐Cheol Han, Mijin Kwon, Seung‐Ho Lee   +5 more
wiley   +1 more source

Amyloid-β impairs mitochondrial dynamics and autophagy in Alzheimer’s disease experimental models

Scientific Reports, 2022
The most accepted hypothesis in Alzheimer’s disease (AD) is the amyloid cascade which establishes that Aβ accumulation may induce the disease development.
Macarena de la Cueva, Desiree Antequera, Lara Ordoñez-Gutierrez, Francisco Wandosell, Antonio Camins, Eva Carro, Fernando Bartolome   +6 more
doaj   +1 more source

Cellular Senescence in Neurodegenerative Diseases

Frontiers in Cellular Neuroscience, 2020
Cellular senescence is a homeostatic biological process characterized by a permanent state of cell cycle arrest that can contribute to the decline of the regenerative potential and function of tissues.
C. Martínez-Cué, N. Rueda
semanticscholar   +1 more source

Prion-induced neurotoxicity: Possible role for cell cycle activity and DNA damage response. [PDF]

, 2015
Protein misfolding neurodegenerative diseases arise through neurotoxicity induced by aggregation of host proteins. These conditions include Alzheimer's disease, Huntington's disease, Parkinson's disease, motor neuron disease, tauopathies and prion ...

core   +1 more source

Neurotoxic amyloid β‐peptide and tau produce cytokine‐like effects on PMCA in glioblastoma cell lines, enhancing its activity and isoforms expression

FEBS Open Bio, EarlyView.
Two biomarkers of Alzheimer's disease, amyloid β‐peptide (Aβ) and tau, induce the transformation of U‐251 and other glioblastoma cell lines into neurotoxic A1‐like reactive astrocytes. This transformation is produced by cytokines and is followed by upregulation of PMCA activity and isoform expression, and is closely associated with inflammation, as ...
María Berrocal, Alberto Alvarez‐Barrientos, Ana M. Mata   +2 more
wiley   +1 more source

CXCR4involvement in neurodegenerative diseases [PDF]

Translational Psychiatry, 2017
ABSTRACTNeurodegenerative diseases likely share common underlying pathobiology. Although prior work has identified susceptibility loci associated with various dementias, few, if any, studies have systematically evaluated shared genetic risk across several neurodegenerative diseases.
Bonham, Luke W, Karch, Celeste M, Ferrari, Raffaele, Danek, A., Van Deerlin, V. M., Grossman, M., Trojanowski, J. Q., van der Zee, J., Cruts, M., Van Broeckhoven, C., Cappa, S. F., Leber, I., Hannequin, D., Hardy, John, Golfier, V., Vercelletto, M., Brice, A., Nacmias, B., Sorbi, S., Bagnoli, S., Piaceri, I., Nielsen, J. E., Hjermind, L. E., Riemenschneider, M., Momeni, Parastoo, Mayhaus, M., Ibach, B., Gasparoni, G., Pichler, S., Gu, W., Rossor, M. N., Fox, N. C., Warren, J. D., Spillantini, M. G., Morris, H. R., Höglinger, Günter, Rizzu, P., Heutink, P., Snowden, J. S., Rollinson, S., Richardson, A., Gerhard, A., Bruni, A. C., Maletta, R., Frangipane, F., Cupidi, C., Müller, Ulrich, Bernardi, L., Anfossi, M., Gallo, M., Conidi, M. E., Smirne, N., Rademakers, R., Baker, M., Dickson, D. W., Graff-Radford, N. R., Petersen, R. C., Hess, Christopher P, Knopman, D., Josephs, K. A., Boeve, B. F., Parisi, J. E., Seeley, W. W., Miller, B. L., Karydas, A. M., Rosen, H., van Swieten, J. C., Dopper, E. G. P., Sugrue, Leo P, Seelaar, H., Pijnenburg, Y. A. L., Scheltens, P., Logroscino, G., Capozzo, R., Novelli, V., Puca, A. A., Franceschi, M., Postiglione, A., Milan, G., Dillon, William P, Sorrentino, P., Kristiansen, M., Chiang, H-H, Graff, C., Pasquier, F., Rollin, A., Deramecourt, V., Lebouvier, T., Kapogiannis, D., Ferrucci, L., Schellenberg, Gerard D, Pickering-Brown, S., Singleton, A. B., Hardy, J., Momeni, P., Miller, Bruce L, Fan, Chun C, Andreassen, Ole A, Dale, Anders M, Barkovich, A James, Yokoyama, Jennifer S, Desikan, Rahul S, Consortium, International FTD-Genomics, Consortium, International Parkinson’s Disease Genetics, Project, International Genomics of Alzheimer’s, Ferrari, R., Hernandez, D. G., Tan, Chin, Nalls, M. A., Rohrer, J. D., Ramasamy, A., Kwok, J. B. J., Dobson-Stone, C., Schofield, P. R., Halliday, G. M., Hodges, J. R., Piguet, O., Bartley, L., Geier, Ethan G, Thompson, E., Haan, E., Hernández, I., Ruiz, A., Boada, M., Borroni, B., Padovani, A., Cruchaga, C., Cairns, N. J., Benussi, L., Wang, Yunpeng, Binetti, G., Ghidoni, R., Forloni, G., Albani, D., Galimberti, D., Fenoglio, C., Serpente, M., Scarpini, E., Clarimón, J., Lleó, A., Wen, Natalie, Blesa, R., Waldö, M Landqvist, Nilsson, K., Nilsson, C., Mackenzie, I. R. A., Hsiung, G-Y R, Mann, D. M. A., Grafman, J., Morris, C. M., Attems, J., Broce, Iris J, Griffiths, T. D., McKeith, I. G., Thomas, A. J., Pietrini, P., Huey, E. D., Wassermann, E. M., Baborie, A., Jaros, E., Tierney, M. C., Pastor, P., Li, Yi, Razquin, C., Ortega-Cubero, S., Alonso, E., Perneczky, R., Diehl-Schmid, J., Alexopoulos, P., Kurz, A., Rainero, I., Rubino, E., Pinessi, L., Barkovich, Matthew J, Rogaeva, E., George-Hyslop, P St, Rossi, G., Tagliavini, F., Giaccone, G., Rowe, J. B., Schlachetzki, J. C. M., Uphill, J., Collinge, J., Mead, S.   +183 more
openaire   +12 more sources

Histone Deacetylases Inhibitors in Neurodegenerative Diseases, Neuroprotection and Neuronal Differentiation

Frontiers in Pharmacology, 2020
Histone deacetylases (HADC) are the enzymes that remove acetyl group from lysine residue of histones and non-histone proteins and regulate the process of transcription by binding to transcription factors and regulating fundamental cellular process such ...
S. Shukla, B. Tekwani
semanticscholar   +1 more source

FEM1B enhances TRAIL‐induced apoptosis in T lymphocytes and monocytes

FEBS Open Bio, EarlyView.
FEM1B facilitates TRAIL‐induced apoptosis through distinct mechanisms in T lymphocytes and monocytes. In T lymphocytes, FEM1B engages with TRAF2, leading to a reduction in TRAF2 expression, which subsequently lessens TRAF2's inhibitory influence on caspase‐8.
Chenbo Yang, Wenhui Yu, Cui Dang, Jingjing Zhang, Jiahan Lu, Jing Xue   +5 more
wiley   +1 more source