Search Within


Applied Filters:
Showing 1-14 of 14 results for "A8326" within Papers
beta APP and furin mRNA concentrates in immature senile plaques in the brain of Alzheimer patients
Marcinkiewicz M
Journal of Neuropathology and Experimental Neurology, 61(9), 815-829 (2002)
The metabolism of beta-amyloid converting enzyme and beta-amyloid precursor protein processing
Benjannet S, et al.
Biochemical and Biophysical Research Communications, 325(1), 235-242 (2004)
Amyloid precursor protein processing and Alzheimer's disease
OBrien RJ and Wong PC
Annual Review of Neuroscience, 34, 185-204 (2011)
Jonathan P T Corcoran et al.
The European journal of neuroscience, 20(4), 896-902 (2004-08-13)
We have disrupted the retinoid signalling pathway in adult rats by a dietary deficiency of vitamin A. After 1 year of this dietary deficiency, there was a deposition of amyloid beta in the cerebral blood vessels. There is a downregulation
Katrine R Lind et al.
Neurochemistry international, 62(5), 784-795 (2013-02-16)
Oxidative-nitrosative stress and inflammatory responses are associated with endoplasmic reticulum (ER) stress in diabetic retinopathy, raising the possibility that disturbances in ER protein processing may contribute to CNS dysfunction in diabetics. Upregulation of the unfolded protein response (UPR) is a
Learning performances, brain NGF distribution and NPY levels in transgenic mice expressing TNF-alpha
Fiore M, et al.
Behavioural Brain Research, 112(1), 165-175 (2000)
A Law et al.
Brain research. Brain research reviews, 35(1), 73-96 (2001-03-14)
Alzheimer's disease (AD) is the most common form of dementia, with progressive cognitive deficits being the primary symptom. AD is neuropathologically characterized by amyloid and neurofibrillary tangle depositions, basal forebrain cholinergic deficit, and extensive neuronal loss and synaptic changes in
S Benjannet et al.
The Journal of biological chemistry, 276(14), 10879-10887 (2001-01-22)
Processing of the beta-amyloid precursor protein (betaAPP) by beta- and gamma-secretases generates the amyloidogenic peptide Abeta, a major factor in the etiology of Alzheimer's disease. Following the recent identification of the beta-secretase beta-amyloid-converting enzyme (BACE), we herein investigate its zymogen
Jhana O Hendrickx et al.
International journal of molecular sciences, 22(13) (2021-07-03)
Increasing epidemiological evidence highlights the association between systemic insulin resistance and Alzheimer's disease (AD). As insulin resistance can be caused by high-stress hormone levels and since hypercortisolism appears to be an important risk factor of AD, we aimed to investigate
Scott B Raymond et al.
PloS one, 3(5), e2175-e2175 (2008-05-15)
Alzheimer's disease is a neurodegenerative disorder typified by the accumulation of a small protein, beta-amyloid, which aggregates and is the primary component of amyloid plaques. Many new therapeutic and diagnostic agents for reducing amyloid plaques have limited efficacy in vivo
Kelly K Ball et al.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 30(1), 162-176 (2009-10-02)
Metabolic brain imaging is widely used to evaluate brain function and disease, and quantitative assays require local retention of compounds used to register changes in cellular activity. As labeled metabolites of [1- and 6-(14)C]glucose are rapidly released in large quantities
Yanfang Rui et al.
Molecular brain, 9(1), 79-79 (2016-08-19)
Small oligomeric forms of amyloid-β (Aβ) are believed to be the culprit for declined brain functions in AD in part through their impairment of neuronal trafficking and synaptic functions. However, the precise cellular actions of Aβ oligomers and underlying mechanisms
Mikko Hiltunen et al.
The Journal of biological chemistry, 281(43), 32240-32253 (2006-09-02)
Ubiquilin 1 (UBQLN1) is a ubiquitin-like protein, which has been shown to play a central role in regulating the proteasomal degradation of various proteins, including the presenilins. We recently reported that DNA variants in UBQLN1 increase the risk for Alzheimer
Yili Wu et al.
Scientific reports, 6, 22460-22460 (2016-03-05)
Down syndrome (DS), caused by trisomy of chromosome 21, is one of the most common genetic disorders. Patients with DS display growth retardation and inevitably develop characteristic Alzheimer's disease (AD) neuropathology, including neurofibrillary tangles and neuritic plaques. The expression of
Page 1 of 1