Results 71 to 80 of about 304,354 (194)

Hypoxic regulation of ion channel function and expression [PDF]

, 2002
Acute hypoxia regulates the activity of specific ion channels in a rapid and reversible manner. Such effects underlie appropriate cellular responses to hypoxia which are designed to initiate cardiorespiratory reflexes and contribute importantly to other ...
Peers, C.
core   +1 more source

GABA and glutamate moderate beta-amyloid related functional connectivity in cognitively unimpaired old-aged adults

NeuroImage: Clinical, 2019
Background: Effects of beta-amyloid accumulation on neuronal function precede the clinical manifestation of Alzheimer's disease (AD) by years and affect distinct cognitive brain networks.
F.C. Quevenco, S.J. Schreiner, M.G. Preti, J.M.G. van Bergen, T. Kirchner, M. Wyss, S.C. Steininger, A. Gietl, S.E. Leh, A. Buck, K.P. Pruessmann, C. Hock, R.M. Nitsch, A. Henning, D. Van De Ville, P.G. Unschuld   +15 more
doaj   +1 more source

Predicting the course of Alzheimer's progression. [PDF]

, 2019
Alzheimer's disease is the most common neurodegenerative disease and is characterized by the accumulation of amyloid-beta peptides leading to the formation of plaques and tau protein tangles in brain.
Aisen, Paul S, Alzheimer’s Disease Neuroimaging Initiative, Donohue, Michael C, Iddi, Samuel, Li, Dan, Rafii, Michael S, Thompson, Wesley K   +6 more
core  

Interactive effects of vascular risk burden and advanced age on cerebral blood flow. [PDF]

, 2014
Vascular risk factors and cerebral blood flow (CBF) reduction have been linked to increased risk of cognitive impairment and Alzheimer's disease (AD); however the possible moderating effects of age and vascular risk burden on CBF in late life remain ...
Bangen, Katherine J, Bondi, Mark W, Clark, Lindsay R, Delano-Wood, Lisa, Dev, Sheena I, Harmell, Alexandrea L, Liu, Thomas T, Nation, Daniel A, Salmon, David P, Wierenga, Christina E, Zlatar, Zvinka Z   +10 more
core   +1 more source

Repurposing the KCa3.1 inhibitor senicapoc for Alzheimer's disease. [PDF]

, 2019
ObjectiveMicroglia play a pivotal role in the initiation and progression of Alzheimer's disease (AD). We here tested the therapeutic hypothesis that the Ca2+-activated potassium channel KCa3.1 constitutes a potential target for treating AD by reducing ...
Bushong, Trevor, Chavez, Monique, Jin, Lee-Way, Lucente, Jacopo Di, Maezawa, Izumi, Nguyen, Hai M, Singh, Latika, Singh, Vikrant, Wulff, Heike   +8 more
core   +2 more sources

The Amyloid Precursor Protein Controls PIKfyve Function [PDF]

PLOS ONE, 2015
While the Amyloid Precursor Protein (APP) plays a central role in Alzheimer's disease, its cellular function still remains largely unclear. It was our goal to establish APP function which will provide insights into APP's implication in Alzheimer's disease.
Balklava, Z, Niehage, C, Currinn, H, Mellor, L, Guscott, B, Poulin, G, Hoflack, B, Wassmer, T.   +7 more
openaire   +4 more sources

A Novel Genetic Screen Identifies Modifiers of Age-Dependent Amyloid β Toxicity in the Drosophila Brain [PDF]

, 2017
The accumulation of amyloid β peptide (Aβ) in the brain of Alzheimer's disease (AD) patients begins many years before clinical onset. Such process has been proposed to be pathogenic through the toxicity of Aβ soluble oligomers leading to synaptic ...
Belfiori Carrasco, Lautaro Francisco, Bocai, Nadia Irina, Castaño, Eduardo Miguel, Ceriani, Maria Fernanda, Marcora, Maria Silvina, Morelli, Laura   +5 more
core   +1 more source

Does the Hfq Protein Contribute to RNA Cargo Translocation into Bacterial Outer Membrane Vesicles?

Pathogens
Gram-negative bacteria release outer membrane vesicles (OMVs) that deliver various molecules, including virulence factors, to interact with their host.
Marisela Velez, Véronique Arluison
doaj   +1 more source

Amyloid prions in fungi [PDF]

, 2016
Prions are infectious protein polymers that have been found to cause fatal diseases in mammals. Prions have also been identified in fungi (yeast and filamentous fungi), where they behave as cytoplasmic non-Mendelian genetic elements.
Aguzzi, Aguzzi, Aigle, Alberti, Aron, Balguerie, Ball, Bardill, Baudin-Baillieu, Baxa, Baxa, Borchsenius, Brachmann, Bradley, Brown, Byers, Cai, Chakrabortee, Chen, Chernoff, Collinge, Coustou, Coustou-Linares, Cox, Daskalov, Daskalov, Daskalov, Daskalov, Derkatch, Derkatch, Derkatch, Diaz-Avalos, DiSalvo, Douglas, Eichner, Espinosa Angarica, Fan, Garcia, Glover, Glover, Gorkovskiy, Griswold, Habenstein, Halfmann, Halfmann, Harrison, Higurashi, Holmes, Huang, Jarosz, Jarosz, Jung, Kabir, Kajava, Kajava, Kelly, King, King, Koch, Kochneva-Pervukhova, Krishnan, Kryndushkin, Kumar, Kunz, Lancaster, Li, Lum, Malato, Masel, Masison, Masison, Mathur, McGlinchey, Mizuno, Nakayashiki, Nelson, Newnam, Ohhashi, Patel, Patino, Paushkin, Prusiner, Rajon, Ritter, Rizet, Roberts, Ross, Ross, Schlieker, Schlumpberger, Sen, Seuring, Shewmaker, Shorter, Sondheimer, Sondheimer, Speldewinde, Stein, Taneja, Tapia, Tessier, Tipton, Tompa, Toyama, True, True, Tsai, Tycko, Tyedmers, Uptain, Van Melckebeke, Verges, Wan, Wasmer, Watts, Westergard, Wickner, Wickner, Wickner, Wickner, Wickner, Wickner, Zhou   +122 more
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Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer's disease. [PDF]

, 2019
Apolipoprotein (apo) E4 is the major genetic risk factor for Alzheimer's disease (AD), increasing risk and decreasing age of disease onset. Many studies have demonstrated the detrimental effects of apoE4 in varying cellular contexts.
Huang, Yadong, Jones, Emily A, Najm, Ramsey   +2 more
core   +1 more source