Results 61 to 70 of about 22,628 (189)

Alzheimer’s disease linked Aβ42 exerts product feedback inhibition on γ-secretase impairing downstream cell signaling

eLife
Amyloid β (Aβ) peptides accumulating in the brain are proposed to trigger Alzheimer’s disease (AD). However, molecular cascades underlying their toxicity are poorly defined.
Katarzyna Marta Zoltowska, Utpal Das, Sam Lismont, Thomas Enzlein, Masato Maesako, Mei CQ Houser, Maria Luisa Franco, Burcu Özcan, Diana Gomes Moreira, Dmitry Karachentsev, Ann Becker, Carsten Hopf, Marçal Vilar, Oksana Berezovska, William Mobley, Lucía Chávez-Gutiérrez   +15 more
doaj   +1 more source

Gains and losses on the road to understanding Alzheimer’s disease

Swiss Medical Weekly, 2015
Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common cause for dementia, which affects approximately 120 thousand people in Switzerland and 35 million worldwide.
Uwe Konietzko
doaj   +1 more source

Discovery of novel benzophenone integrated derivatives as anti-Alzheimer's agents targeting presenilin-1 and presenilin-2 inhibition: A computational approach.

PLoS ONE, 2022
The most commonly accepted hypothesis of Alzheimer's disease (AD) is the amyloid hypothesis caused due to formation of accumulation of Aβ42 isoform, which leads to neurodegeneration.
Reshma Mary Martiz, Shashank M Patil, Ramith Ramu, Jayanthi M K, Ashwini P, Lakshmi V Ranganatha, Shaukath Ara Khanum, Ekaterina Silina, Victor Stupin, Raghu Ram Achar   +9 more
doaj   +1 more source

Clustering Properties of Neuronal Ryanodine Receptor 2 and Remodeling in the APP/PS1 Mouse Model of Alzheimer's Disease

Acta Physiologica, Volume 242, Issue 7, July 2026.
ABSTRACT Aim The ryanodine receptor (RyR2) is an intracellular Ca2+ release channel which mediates numerous cellular functions across different tissues. Dysregulation of RyR2 channel activity leads to pathological Ca2+ release, which often underlies disrupted cellular signaling in disease states.
Michelle L. Munro, Ruben Vergara Silva, Shane M. Ohline, Ei Phyo Khaing, Joan A. Chan, Mohamed F. Ibrahim, Tausi F. Tausi, Wickliffe C. Abraham, Peter P. Jones   +8 more
wiley   +1 more source

Pathological and physiological functions of presenilins [PDF]

Molecular Neurodegeneration, 2006
Abstract Mutations in PSEN1 and PSEN2 genes account for the majority of cases of early-onset familial Alzheimer disease. Since the first prediction of a genetic link between PSEN1 and PSEN2 with Alzheimer's disease, many research groups from both academia and pharmaceutical industry have sought to unravel how pathogenic mutations in PSEN ...
Vetrivel, K. S., Zhang, Y. W., Xu, H. X., Thinakaran, G.   +3 more
openaire   +3 more sources

Presenilin-mediated cleavage of APP regulates synaptotagmin-7 and presynaptic plasticity

Nature Communications, 2018
Mutations in presenilin, which cleaves amyloid precursor protein, cause familial Alzheimer’s Disease. Here, the authors show that loss of presenilin leads to loss of synaptotagmin 7, leading to impaired presynaptic release.
Gaël Barthet, Tomàs Jordà-Siquier, Julie Rumi-Masante, Fanny Bernadou, Ulrike Müller, Christophe Mulle   +5 more
doaj   +1 more source

How γ-secretase hits a moving target

eLife, 2016
An improved understanding of the ways that amyloid-beta peptides are formed could help efforts to find a treatment for Alzheimer’s disease.
Charles R Sanders
doaj   +1 more source

Small Extracellular Vesicles from Neural Cells: Physiological and Pathological Roles, and Potential in Neurodegenerative Therapy

Advanced Healthcare Materials, Volume 15, Issue 21, 5 June 2026.
Neural cell–derived small extracellular vesicles (sEVs) are emerging as pivotal mediators in neurodegenerative diseases, exerting both pathogenic and therapeutic functions. This review synthesizes current evidence on how sEVs from distinct neural cell types regulate neurodegeneration, neuroprotection, biomarker discovery, and targeted drug delivery ...
Muhammad Waqas Salim, Wei Zhang, Lyndsey Collins‐Praino, Yuling Wang, Andrew Care   +4 more
wiley   +1 more source

Stable neuronal representations underlie cognitive resilience to Alzheimer's disease pathology

Alzheimer's &Dementia, Volume 22, Issue 6, June 2026.
Abstract INTRODUCTION While Alzheimer's disease (AD) typically elicits progressive cognitive decline, some individuals with significant AD pathology maintain cognition. Understanding the neuronal underpinnings of such cognitive resilience would propel the development of interventions for delaying dementia.
Keying Chen, Emma Pineau, Margaret Koletar, Andrea Trevisiol, Jack Simiao He, Mary Hill, Maged Goubran, John Sled, JoAnne McLaurin, Bojana Stefanovic   +9 more
wiley   +1 more source

18F-FDG-PET in Mouse Models of Alzheimer's Disease

Frontiers in Medicine, 2019
Suitable animal models and in vivo biomarkers are essential for development and evaluation of new therapeutic strategies in Alzheimer's disease (AD). 18F-Fluorodeoxyglucose (18F-FDG)-positron-emission tomography (PET) is an imaging biomarker that allows ...
Caroline Bouter, Yvonne Bouter
doaj   +1 more source