Results 21 to 30 of about 4,375,511 (236)

Destruxin E Decreases Beta-Amyloid Generation by Reducing Colocalization of Beta-Amyloid-Cleaving Enzyme 1 and Beta-Amyloid Protein Precursor [PDF]

open access: yes, 2009
Alzheimer-disease-associated beta-amyloid (A beta) is produced by sequential endoproteolysis of beta-amyloid protein precursor (beta APP): the extracellular portion is shed by cleavage in the juxtamembrane region by beta-amyloid-cleaving enzyme (BACE ...
Nakano, Yuko   +27 more
core   +1 more source

Pro-domain removal in ASP-2 and the cleavage of the amyloid precursor are influenced by pH. [PDF]

open access: yes, 2002
BACKGROUND: One of the signatures of Alzheimer's disease is the accumulation of aggregated amyloid protein, Abeta, in the brain. Abeta arises from cleavage of the Amyloid Precursor protein by beta and gamma secretases, which present attractive candidates
Brian Austen   +5 more
core   +1 more source

Rosiglitazone ameliorates diffuse axonal injury by reducing loss of tau and up-regulating caveolin-1 expression

open access: yesNeural Regeneration Research, 2016
Rosiglitazone up-regulates caveolin-1 levels and has neuroprotective effects in both chronic and acute brain injury. Therefore, we postulated that rosiglitazone may ameliorate diffuse axonal injury via its ability to up-regulate caveolin-1, inhibit ...
Yong-lin Zhao   +5 more
doaj   +1 more source

Platelet APP Processing: Is It a Tool to Explore the Pathophysiology of Alzheimer’s Disease? A Systematic Review

open access: yesLife, 2021
The processing of the amyloid precursor protein (APP) is a critical event in the formation of amyloid plaques. Platelets contain most of the enzymatic machinery required for APP processing and correlates of intracerebral abnormalities have been ...
Manuel Glauco Carbone   +4 more
doaj   +1 more source

Exercise for the prevention of Alzheimer's disease: Multiple pathways to promote non-amyloidogenic AβPP processing

open access: yesAging and Health Research, 2022
With advancements in our ability to treat or manage more diseases than ever, people are able to live longer in greater health. However, for individuals who develop Alzheimer's disease (AD), therapeutic options are currently limited to symptom management ...
Richard J. Elsworthy   +3 more
doaj   +1 more source

Amyloid oligomer conformation in a group of natively folded proteins. [PDF]

open access: yesPLoS ONE, 2008
Recent in vitro and in vivo studies suggest that destabilized proteins with defective folding induce aggregation and toxicity in protein-misfolding diseases.
Yuji Yoshiike   +5 more
doaj   +1 more source

Minocycline corrects early, pre-plaque neuroinflammation and inhibits BACE-1 in a transgenic model of Alzheimer's disease-like amyloid pathology

open access: yesJournal of Neuroinflammation, 2012
Background A growing body of evidence indicates that inflammation is one of the earliest neuropathological events in Alzheimer's disease. Accordingly, we have recently shown the occurrence of an early, pro-inflammatory reaction in the hippocampus of ...
Ferretti Maria   +4 more
doaj   +1 more source

Altered amyloid precursor protein processing regulates glucose uptake and oxidation in cultured rodent myotubes [PDF]

open access: yes, 2014
Aims/hypothesis: Impaired glucose uptake in skeletal muscle is an important contributor to glucose intolerance in type 2 diabetes. The aspartate protease, beta-site APP-cleaving enzyme 1 (BACE1), a critical regulator of amyloid precursor protein (APP ...
Hamilton, D. Lee   +26 more
core   +1 more source

Microbiome‐blood–brain barrier interactions in aging — mechanisms and therapeutic potential

open access: yesFEBS Letters, EarlyView.
Aging reshapes the gut microbiome (↓SCFA‐producing commensals; ↑pro‐inflammatory outputs), shifting circulating metabolites (↓SCFAs; ↑LPS, ↑TMAO, ↑PAA) that act at the BBB to increase nonspecific transcytosis, alter transport, and promote astrocyte reactivity, heightening brain vulnerability.
Daniel Cuervo‐Zanatta   +3 more
wiley   +1 more source

Treatment with KCL‐286, a first‐in‐class retinoic acid receptor‐β (RARβ) agonist, ameliorates neuronal DNA damage and inflammation in a mouse model of Alzheimer's disease

open access: yesFEBS Open Bio, EarlyView.
Repair of neuronal DNA damage in Alzheimer's disease by KCL‐286. (A) Amyloid‐β oligomers and plaques impair neuronal DNA repair pathways, leading to DNA double‐strand breaks and glial activation. (B) KCL‐286 activates RARβ/RXR signalling via retinoic acid response elements (RAREs), associated with increased BRCA1 expression, enhanced DNA repair and ...
Natasha Hill   +6 more
wiley   +1 more source

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