Results 1 to 10 of about 20,406 (139)

Presenilin L166P Mutation, a Model of Familial Alzheimer's Disease, Leads to Early Onset Bone Loss. [PDF]

open access: yesCompr Physiol
Female‐specific bone loss in Alzheimer's disease mouse models: There is a significant alteration of bone phenotype during Alzheimer's disease. Using integrated imaging and biological assays, we observed changes in the bone microarchitecture, composition, and function in PSEN K1 and PSEN1/hAPP Tg+ mice, predominantly in the females. ABSTRACT Accelerated
Suryadevara V   +12 more
europepmc   +2 more sources

The orphan drug dichloroacetate reduces amyloid beta-peptide production whilst promoting non-amyloidogenic proteolysis of the amyloid precursor protein.

open access: yesPLoS ONE, 2022
The amyloid cascade hypothesis proposes that excessive accumulation of amyloid beta-peptides is the initiating event in Alzheimer's disease. These neurotoxic peptides are generated from the amyloid precursor protein via sequential cleavage by β- and γ ...
Edward T Parkin   +3 more
doaj   +1 more source

Altered processing of amyloid precursor protein in cells undergoing apoptosis. [PDF]

open access: yesPLoS ONE, 2013
Altered proteolysis of amyloid precursor protein is an important determinant of pathology development in Alzheimer's disease. Here, we describe the detection of two novel fragments of amyloid precursor protein in H4 neuroglioma cells undergoing apoptosis.
Tina Fiorelli   +2 more
doaj   +1 more source

A thermodynamic investigation of amyloid precursor protein processing by human γ-secretase

open access: yesCommunications Biology, 2022
Thermodynamic analysis from unbiased molecular dynamics and bias-exchange metadynamics simulations reveals possible mechanisms on how γ-secretase cleaves the transmembrane domains of amyloid precursor protein into amyloid-β peptides.
Xiaoli Lu, Jing Huang
doaj   +1 more source

Targeting Amyloidogenic Processing of APP in Alzheimer’s Disease

open access: yesFrontiers in Molecular Neuroscience, 2020
Alzheimer’s disease (AD) is the most common type of senile dementia, characterized by neurofibrillary tangle and amyloid plaque in brain pathology. Major efforts in AD drug were devoted to the interference with the production and accumulation of amyloid ...
Jing Zhao   +7 more
doaj   +1 more source

Generation of amyloid-β is reduced by the interaction of calreticulin with amyloid precursor protein, presenilin and nicastrin.

open access: yesPLoS ONE, 2013
Dysregulation of the proteolytic processing of amyloid precursor protein by γ-secretase and the ensuing generation of amyloid-β is associated with the pathogenesis of Alzheimer's disease.
Nina Stemmer   +9 more
doaj   +1 more source

Determination of the proteolytic cleavage sites of the amyloid precursor-like protein 2 by the proteases ADAM10, BACE1 and γ-secretase. [PDF]

open access: yesPLoS ONE, 2011
Regulated intramembrane proteolysis of the amyloid precursor protein (APP) by the protease activities α-, β- and γ-secretase controls the generation of the neurotoxic amyloid β peptide.
Sebastian Hogl   +3 more
doaj   +1 more source

Ablation of Prion Protein in Wild Type Human Amyloid Precursor Protein (APP) Transgenic Mice Does Not Alter The Proteolysis of APP, Levels of Amyloid-β or Pathologic Phenotype.

open access: yesPLoS ONE, 2016
The cellular prion protein (PrPC) has been proposed to play an important role in the pathogenesis of Alzheimer's disease. In cellular models PrPC inhibited the action of the β-secretase BACE1 on wild type amyloid precursor protein resulting in a ...
Isobel J Whitehouse   +7 more
doaj   +1 more source

Probing Mechanisms and Therapeutic Potential of γ-Secretase in Alzheimer’s Disease

open access: yesMolecules, 2021
The membrane-embedded γ-secretase complex carries out hydrolysis within the lipid bilayer in proteolyzing nearly 150 different membrane protein substrates.
Michael S. Wolfe
doaj   +1 more source

Specific Inhibition of β-Secretase Processing of the Alzheimer Disease Amyloid Precursor Protein

open access: yesCell Reports, 2016
Development of disease-modifying therapeutics is urgently needed for treating Alzheimer disease (AD). AD is characterized by toxic β-amyloid (Aβ) peptides produced by β- and γ-secretase-mediated cleavage of the amyloid precursor protein (APP).
Saoussen Ben Halima   +10 more
doaj   +1 more source

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