Results 111 to 120 of about 14,107 (263)

Constitutive α- and β-secretase cleavages of the amyloid precursor protein are partially coupled in neurons, but not in frequently used cell lines

Neurobiology of Disease, 2013
Proteolytic cleavage of the amyloid precursor protein (APP) by the two proteases α- and β-secretases controls the generation of the amyloid β peptide (Aβ), a key player in Alzheimer's disease pathogenesis. The α-secretase ADAM10 and the β-secretase BACE1
Alessio Colombo, Huanhuan Wang, Peer-Hendrik Kuhn, Richard Page, Elisabeth Kremmer, Peter J. Dempsey, Howard C. Crawford, Stefan F. Lichtenthaler   +7 more
doaj   +1 more source

CD74 interacts with APP and suppresses the production of Aβ [PDF]

, 2009
Background Alzheimer disease (AD) is characterized by senile plaques, which are mainly composed of β amyloid (Aβ) peptides. Aβ is cleaved off from amyloid precursor protein (APP) with consecutive proteolytic processing by β-secretase and γ-secretase ...
D'Adamio Luciano, Matsuda Yukiko, Matsuda Shuji   +2 more
core   +1 more source

Analyzing Nicotine Action Against Amyloid Toxicity by NMR‐Pharmacometabolomics: An Exploratory Study

NMR in Biomedicine, Volume 39, Issue 4, April 2026.
Combined metabolomic analysis of the intracellular and extracellular portions of SH‐SY5Y cells revealed that, in the presence of Aβ 1–42, nicotine primarily influences pathways related to neurotransmission, energy metabolism, as well as the biosynthesis and degradation of membrane phospholipids.
Enza Napolitano, Carmen Marino, Manuela Grimaldi, Michela Buonocore, Angelo Santoro, Anna Maria D'Ursi   +5 more
wiley   +1 more source

Toxic mechanisms of amyloid oligomers and therapeutic strategies

Protein Science, Volume 35, Issue 4, April 2026.
Abstract Amyloid oligomers are increasingly recognized as the major toxic contributors across protein‐misfolding disorders. In this review, we cover mechanistic evidence showing how these transient and structurally heterogeneous oligomers disrupt cellular homeostasis by: (i) permeabilizing lipid membranes and forming ion‐conducting pores; (ii ...
Magdalena I. Ivanova, Carmelo La Rosa, Ayyalusamy Ramamoorthy   +2 more
wiley   +1 more source

The multifaceted roles of the transcription factor SP1 in the pathogenesis of Alzheimer's disease: From molecular regulation to therapeutic targets

Alzheimer's &Dementia: Translational Research &Clinical Interventions, Volume 12, Issue 2, April/June 2026.
Abstract Alzheimer's disease (AD) is driven by interrelated pathologies, including the accumulation of amyloid β (Aβ), tau pathology, chronic neuroinflammation, and oxidative stress (OS). These pathological processes collectively lead to progressive neurodegeneration.
Zhengxiang Lv, Xiaodong Liu, Qin Huang, Haijun Liu, Zucai Xu, Ping Xu   +5 more
wiley   +1 more source

Alzheimer's disease drug development pipeline: 2026

Alzheimer's &Dementia: Translational Research &Clinical Interventions, Volume 12, Issue 2, April/June 2026.
Abstract INTRODUCTION Discovery and development of new therapies for Alzheimer's disease (AD) are urgently needed to address the world's growing population of individuals on the AD pathophysiological continuum. Clinicaltrials.gov is a resource for studying drugs in development for treatment of AD. RESULTS There are currently 158 drugs in 192 AD trials.
Jeffrey L. Cummings, Yadi Zhou, Yuxin Yang, Kate Zhong, Jorge Fonseca, Amanda Leisgang Osse, Feixiong Cheng   +6 more
wiley   +1 more source

Cellular basis of Alzheimer′s disease

Annals of Indian Academy of Neurology, 2010
Alzheimer′s disease (AD) is the most common form of neurodegenerative disease. A characteristic feature of the disease is the presence of amyloid-β (Aβ) which either in its soluble oligomeric form or in the plaque-associated form is ...
Bali Jitin, Halima Saoussen, Felmy Boas, Goodger Zoe, Zurbriggen Sebastian, Rajendran Lawrence   +5 more
doaj  

Modulation of β-amyloid precursor protein trafficking and processing by the low density lipoprotein receptor family

Molecular Neurodegeneration, 2006
Amyloid-β peptide (Aβ) accumulation in the brain is an early, toxic event in the pathogenesis of Alzheimer's disease (AD). Aβ is produced by proteolytic processing of a transmembrane protein, β-amyloid precursor protein (APP), by β- and γ-secretases ...
Cam Judy A, Bu Guojun
doaj   +1 more source

Familial Alzheimer’s disease mutations in amyloid protein precursor alter proteolysis by γ-secretase to increase amyloid β-peptides of ≥45 residues [PDF]

, 2021
Sujan Devkota, Todd D. Williams, Michael S. Wolfe   +2 more
openalex   +1 more source

Gene–Environment Interactions for Alzheimer's Disease Pathology in Cognitively Normal Adults: The CABLE Study

European Journal of Neurology, Volume 33, Issue 4, April 2026.
This study investigated gene–environment interactions in Alzheimer's disease (AD) pathology among 1007 cognitively normal adults from the CABLE cohort. Higher AD polygenic risk scores were associated with increased amyloidosis, with significant interactions observed between genetic risk and three modifiable factors—anemia, gingivitis, and anxiety—in ...
Ze‐Xin Guo, Xiao‐Yu He, Yi‐Jun Ge, Bing Zhao, Liang‐Yu Huang, Shi‐Dong Chen, Yan Fu, Pei‐Yang Gao, Ze‐Hu Sheng, Yi‐Ming Huang, Qiong‐Yao Li, Lan Tan   +11 more
wiley   +1 more source