Results 111 to 120 of about 40,397 (225)

Direct association of presenilin‐1 with β‐catenin

open access: yesFEBS Letters, 1998
Families bearing mutations in the presenilin‐1 (PS1) gene develop Alzheimer's disease (AD). However, the mechanism through which PS1 causes AD is unclear. The co‐immunoprecipitation with PS1 in transfected COS‐7 cells indicates that PS1 directly interacts with endogenous β‐catenin, and the interaction requires residues 322–450 of PS1 and 445–676 of β ...
Murayama, Miyuki   +9 more
openaire   +2 more sources

Effect of cold and warm white light on selected endocrine and immune parameters of broiler embryos and hatchlings

open access: yesCzech Journal of Animal Science, 2020
Lighting conditions during incubation can influence embryonic development, post-hatching ontogeny and production efficiency. Previous studies revealed that different light colours differently affect pineal melatonin biosynthesis in embryos and ...
Angelika Drozdova   +2 more
doaj   +1 more source

Altered brain energetics induces mitochondrial fission arrest in Alzheimer's Disease. [PDF]

open access: yes, 2016
Altered brain metabolism is associated with progression of Alzheimer's Disease (AD). Mitochondria respond to bioenergetic changes by continuous fission and fusion.
Bachmeier, Benjamin V   +15 more
core   +1 more source

Pathogenic Neurofibromatosis type 1 gene variants in tumors of non‐NF1 patients and role of R1276

open access: yesFEBS Open Bio, Volume 16, Issue 4, Page 803-813, April 2026.
Somatic variants of the neurofibromatosis type 1 (NF1) gene occur across neoplasms without clinical manifestation of the disease NF1. We identified emerging somatic pathogenic NF1 variants and hotspots, for example, at the arginine finger 1276. Those missense variants provide fundamental information about neurofibromin's role in cancer.
Mareike Selig   +7 more
wiley   +1 more source

Imaging Alzheimer's genetic risk using diffusion MRI: A systematic review

open access: yesNeuroImage: Clinical, 2020
Diffusion magnetic resonance imaging (dMRI) is an imaging technique which probes the random motion of water molecules in tissues and has been widely applied to investigate changes in white matter microstructure in Alzheimer’s Disease.
Judith R. Harrison   +6 more
doaj   +1 more source

Treatment of Alzheimer's Disease with Anti-Homocysteic acid Antibody [PDF]

open access: yes, 2008
Homocysteic acid (HA) may play an important role in Alzhiemer disease (AD) as we previously reported that HA induced accumulation of intraneuronal A[beta]42. In this study, we first analyzed HA levels in a mouse model of AD.
Frank M. LaFerla   +3 more
core   +3 more sources

Characterisation of cytoskeletal abnormalities in mice transgenic for wild-type human tau and familial Alzheimer's disease mutants of APP and presenilin-1

open access: yesNeurobiology of Disease, 2004
To study the role of Aβ amyloid deposits in the generation of cytoskeletal lesions, we have generated a transgenic mouse line coexpressing in the same neurons a wild-type human tau isoform (0N3R), a mutant form of APP (751SL) and a mutant form of PS1 ...
Allal Boutajangout   +6 more
doaj   +1 more source

Neurodegeneration: Potential Causes, Prevention, and Future Treatment Options [PDF]

open access: yes, 2011
Here I advance a hypothesis that neurodegeneration is a natural process associated with aging due to the loss of genetic redundancy following a mathematical model R(t) = R0(1-αe(βC+γI+δEt)t), where the calorie intake (C) and ...
Zhongtao Zhang
core   +2 more sources

γ-Secretase Modulators and Presenilin 1 Mutants Act Differently on Presenilin/γ-Secretase Function to Cleave Aβ42 and Aβ43

open access: yesCell Reports, 2013
Deciphering the mechanism by which the relative Aβ42(43) to total Aβ ratio is regulated is central to understanding Alzheimer disease (AD) etiology; however, the mechanisms underlying changes in the Aβ42(43) ratio caused by familial mutations and γ ...
Masayasu Okochi   +8 more
doaj   +1 more source

APP-BP1 inhibits Aβ42 levels by interacting with Presenilin-1

open access: yesMolecular Neurodegeneration, 2007
Background The β-amyloid precursor protein (APP) is sequentially cleaved by the β- and then γ-secretase to generate the amyloid β-peptides Aβ40 and Aβ42. Increased Aβ42/Aβ40 ratios trigger amyloid plaque formations in Alzheimer's disease (AD).
Neve Rachael L   +5 more
doaj   +1 more source

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