Results 31 to 40 of about 120,581 (311)

Alzheimer's disease-like neuropathology of gene-targeted APP-SLxPS1mut mice expressing the amyloid precursor protein at endogenous levels

open access: yesNeurobiology of Disease, 2005
Most transgenic mice used for preclinical evaluation of potential disease-modifying treatments of Alzheimer's disease develop major histopathological features of this disease by several-fold overexpression of the human amyloid precursor protein.
Christoph Köhler   +3 more
doaj   +1 more source

Amyloid Precursor Protein (APP) and GABAergic Neurotransmission

open access: yesCells, 2019
The amyloid precursor protein (APP) is the parent polypeptide from which amyloid-beta (Aβ) peptides, key etiological agents of Alzheimer’s disease (AD), are generated by sequential proteolytic processing involving β- and γ-secretases.
Bor Luen Tang
doaj   +1 more source

Pro-inflammatory interleukin-18 increases Alzheimer’s disease-associated amyloid-β production in human neuron-like cells [PDF]

open access: yes, 2012
Background: Alzheimer’s disease (AD) involves increased accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles as well as neuronal loss in various regions of the neocortex.
Anderson, G.   +14 more
core   +1 more source

Amyloid precursor protein processing and bioenergetics [PDF]

open access: yesBrain Research Bulletin, 2017
The processing of amyloid precursor protein (APP) to amyloid beta (Aβ) is of great interest to the Alzheimer's disease (AD) field. Decades of research define how APP is altered to form Aβ, and how Aβ generates oligomers, protofibrils, and fibrils. Numerous signaling pathways and changes in cell physiology are known to influence APP processing. Existing
Heather M. Wilkins, Russell H. Swerdlow
openaire   +2 more sources

Dual Action of Memantine in Alzheimer Disease: A Hypothesis

open access: yesTaiwanese Journal of Obstetrics & Gynecology, 2009
Objective: In this study, we proposed a hypothesis to explain the mechanisms of memantine action in treating Alzheimer disease (AD). Memantine may reduce the expression of amyloid precursor protein and tau protein, as well as acting as an antagonist of N-
Tzong-Yuan Wu, Chih-Ping Chen
doaj   +1 more source

Enzymatic Screening of β-Amyloid Precursor Protein-Based Substrates

open access: yesCompounds, 2023
We performed an enzymatic screening of synthetic peptides based on β-amyloid precursor protein substrates. The template peptide sequence was a decapeptide derived from our previous screening study, which determined several effective unnatural amino acids.
Reo Yamada   +5 more
doaj   +1 more source

APP Expression in Primary Neuronal Cell Cultures fromP6 Mice during in vitro Differentiation [PDF]

open access: yes, 1993
Primary neuronal cell cultures from P6 mice were investigated in order to study amyloid protein precursor (APP) gene expression in differentiating neurons.
Sandbrink, R.   +5 more
core   +1 more source

Amyloid precursor protein in pancreatic islets [PDF]

open access: yesJournal of Endocrinology, 2017
The amyloid precursor protein (APP) has been extensively investigated for its role in the production of amyloid beta (Aβ), a plaque-forming peptide in Alzheimer’s disease (AD). Epidemiological evidence suggests type 2 diabetes is a risk factor for AD. The pancreas is an essential regulator of blood glucose levels through the secretion of the hormones ...
Joshua A, Kulas   +2 more
openaire   +2 more sources

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

A Novel Protocol to Quantitatively Measure the Endocytic Trafficking of Amyloid Precursor Protein (APP) in Polarized Primary Neurons with Sub-cellular Resolution

open access: yesBio-Protocol, 2017
Alzheimer’s disease’s established primary trigger is β-amyloid (Aβ) (Mucke and Selkoe, 2012). The amyloid precursor protein (APP) endocytosis is required for Aβ generation at early endosomes (Rajendran and Annaert, 2012).
Florent Ubelmann   +2 more
doaj   +1 more source

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