Results 31 to 40 of about 42,007 (233)

When, where and how? Focus on neuronal calcium dysfunctions in Alzheimer's Disease. [PDF]

, 2016
Alzheimer\u2019s disease (AD), since its characterization as a precise form of dementia with its own pathological hallmarks, has captured scientists\u2019 attention because of its complexity.
AGOSTINI, MARIO, FASOLATO, CRISTINA
core   +1 more source

Presenilin: RIP and beyond [PDF]

Seminars in Cell & Developmental Biology, 2009
Over the years the presenilins (PSENs), a family of multi-transmembrane domain proteins, have been ascribed a number of diverse potential functions. Recent in vivo evidence has supported the existence of PSEN functions beyond its well-established role in regulated intramembrane proteolysis. In this review, we will briefly discuss the ability of PSEN to
Matthew R, Hass, Chihiro, Sato, Raphael, Kopan, Guojun, Zhao   +3 more
openaire   +2 more sources

Calcium in the initiation, progression and as an effector of Alzheimer's disease pathology. [PDF]

, 2009
The cause(s) of sporadic Alzheimer's disease (sAD) are complex and currently poorly understood. They likely result from a combination of genetic, environmental, proteomic and lipidomic factors that crucially occur only in the aged brain.
Green, Kim N
core   +1 more source

Cholestenoic acid, an endogenous cholesterol metabolite, is a potent γ-secretase modulator. [PDF]

, 2015
BackgroundAmyloid-β (Aβ) 42 has been implicated as the initiating molecule in the pathogenesis of Alzheimer's disease (AD); thus, therapeutic strategies that target Aβ42 are of great interest.
Akula, Rajender, Ba, Saritha, Ceballos-Diaz, Carolina, Felsenstein, Kevin M, Golde, Todd E, Hochhaus, Günther, Jung, Joo In, Koo, Edward H, Ladd, Thomas B, Park, Hyo-Jin, Price, Ashleigh R, Ran, Yong, Shapiro, Gideon, Smithson, Lisa A, Tang, Yufei   +14 more
core   +3 more sources

Presenilin‐directed inhibitors of γ‐secretase trigger caspase 3 activation in presenilin‐expressing and presenilin‐deficient cells [PDF]

Journal of Neurochemistry, 2004
AbstractThe amyloid β peptide (Aβ) is generated by subsequent cleavages by β‐ and γ‐secretases. Therefore, these two enzymes are putative therapeutic targets to prevent Aβ production, and hopefully to slow down or even stop the Alzheimer's disease (AD) neurodegenerative process.
Cristine, Alves da Costa, Erwan, Ayral, Jean-François, Hernandez, Peter, St George-Hyslop, Frédéric, Checler   +4 more
openaire   +2 more sources

miRNA-based rapid differentiation of purified neurons from hPSCs advancestowards quick screening for neuronal disease phenotypes in vitro [PDF]

, 2020
Obtaining differentiated cells with high physiological functions by an efficient, but simple and rapid differentiation method is crucial for modeling neuronal diseases in vitro using human pluripotent stem cells (hPSCs).
Aoyama, Takeshi, Ishikawa, Mitsuru, Miyoshi, Hiroyuki, Morota, Saori, Nakamura, Mari, Okano, Hideyuki, Shibata, Shoichiro, Sone, Takefumi, Uchino, Hiroyuki, Watanabe, Hirotaka, Yoo, Andrew S   +10 more
core   +2 more sources

Pen2 and Presenilin-1 Modulate the Dynamic Equilibrium of Presenilin-1 and Presenilin-2 γ-Secretase Complexes [PDF]

Journal of Biological Chemistry, 2009
gamma-Secretase is known to play a pivotal role in the pathogenesis of Alzheimer disease through production of amyloidogenic Abeta42 peptides. Early onset familial Alzheimer disease mutations in presenilin (PS), the catalytic core of gamma-secretase, invariably increase the Abeta42:Abeta40 ratio.
Lisa, Placanica, Leonid, Tarassishin, Guangli, Yang, Erica, Peethumnongsin, Seong-Hun, Kim, Hui, Zheng, Sangram S, Sisodia, Yue-Ming, Li   +7 more
openaire   +2 more sources

Presenilin 2 overexpression is associated with apoptosis in Neuro2a cells

Translational Neuroscience, 2016
Presenilin 1 (PS1) and PS2 are evolutionarily conserved transmembrane proteins of the aspartyl protease family. Initially, they were reported to be associated with the early onset of familial, early-onset Alzheimer’s disease.
Kumar Ashish, Sivanandam T. M., Thakur M. K.   +2 more
doaj   +1 more source

Generation and deposition of Aβ43 by the virtually inactive presenilin‐1 L435F mutant contradicts the presenilin loss‐of‐function hypothesis of Alzheimer's disease

EMBO Molecular Medicine, 2016
As stated by the prevailing amyloid cascade hypothesis, Alzheimer's disease (AD) is caused by the aggregation and cerebral deposition of long amyloid‐β peptide (Aβ) species, which are released from a C‐terminal amyloid precursor protein fragment by γ ...
Benedikt Kretner, Johannes Trambauer, Akio Fukumori, Janina Mielke, Peer‐Hendrik Kuhn, Elisabeth Kremmer, Armin Giese, Stefan F Lichtenthaler, Christian Haass, Thomas Arzberger, Harald Steiner   +10 more
doaj   +1 more source

A γ-secretase inhibitor, but not a γ-secretase modulator, induced defects in BDNF axonal trafficking and signaling: evidence for a role for APP. [PDF]

, 2015
Clues to Alzheimer disease (AD) pathogenesis come from a variety of different sources including studies of clinical and neuropathological features, biomarkers, genomics and animal and cellular models. An important role for amyloid precursor protein (APP)
Cheng, Soan, Goldstein, Lawrence SB, Mobley, William C, Natera-Naranjo, Orlangie, Nguyen, Phuong, Pearn, Matthew L, Reyna, Sol M, Tanzi, Rudolph E, Wagner, Steven L, Weissmiller, April M, Wu, Chengbiao, Zhao, Xiaobei   +11 more
core   +2 more sources