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We identified psen1 as a regulator of the development of histaminergic neurons in zebrafish
These results suggest that Psen2 (show PSEN2 Proteins) plays a more prominent role in Notch (show NOTCH1 Proteins) signalling and embryo development in zebrafish than in mammals, and that the effect of reduced Psen2 (show PSEN2 Proteins) can be ameliorated by Psen1 loss.
These findings identify Syt1 (show SYT1 Proteins) as a novel Ca(2 (show CA2 Proteins)+)-sensitive PS1 modulator that could regulate synaptic ABETA (show APP Proteins), opening avenues for novel and selective synapse targeting therapeutic strategies.
Expression of mutated presenilin 1 (PS1M146V) in astrocytes alters vesicle dynamics and reduces evoked secretion of the signaling molecule ANP (show NPPA Proteins); both may contribute to the development of Alzheimer disease
PS1(exon8) interacts with nicastrin (show NCSTN Proteins), participating in the gamma-secretase complex formation.
Preclinical cognitive decline was evident in PSEN1 E280A mutation carriers with autosomal dominant Alzheimer's Disease.
most of familial that most of familial Alzheimer's disease-connected mutations in PS1 are loss-of-fu (show UBXN11 Proteins)nction-connected mutations in PS1 are loss-of-function
The chemical properties of PSEN1 variants were computed and correlated against clinical age of symptom onset. Loss of stability and hydrophobicity and gain of polarity relate to disease onset. Mutants impair the membrane structure of PSEN1.
A mutation (c.488A>G, p.His163Arg) of PSEN1 gene was found in a Chinese family affected with early-onset familial Alzheimer's disease (EOFAD).
This report showed that a novel PSEN1 mutation (P267A) and strong evidence for its pathogenicity.
the PS1 Thr147Ile substitution in Alzheimer's disease expands the clinical phenotype to include expressive aphasia and very early onset of dementia
This study identified variants in PSEN1 across a range of phenotypes (Alzheimer's Disease , Alzheimer's Disease and cerebrovascular disease,frontotemporal dementia and progressive supranuclear palsy.
the G206D mutation reduced presenilin-1-presenilin enhancer 2 (show PSENEN Proteins) interaction, but did not abolish gamma-secretase formation and presenilin-1 endoproteolysis
This study deals with the effect of attenuated endoproteolysis of PS1 on store-operated calcium (SOC (show UBXN11 Proteins)) entry in neuronal cells and mouse fibroblasts with double knockouts of PS1 and PS2 (show PDCD6 Proteins)
Results showed that epigenetic mechanisms play a pivotal role in transcriptional regulation of PS1 and PS2 (show PDCD6 Proteins) during cerebral cortical development
lactate levels remained elevated with age and increased aerobic glycolysis enzyme expression correlated with poorer memory performance in APP (show APP Proteins)/PS1 mice
PS1 deficiency depletes vATPase (show ATP6V1H Proteins), impairing lysosomal acidification and calcium homeostasis.
Abeta (show APP Proteins) oligomers in the cerebrospinal fluid (CSF (show CSF2 Proteins)) further promoted the expression of APH-1alpha/-1beta (by >2.5-fold), which enhances the gamma-cleavage of APP (show APP Proteins) and Abeta (show APP Proteins) deposition during AD progression
This study presents novel evidence for the differential expression of PS proteins in a nongenetic model for aging, resulting in an overall increase of the PS2 (show PDCD6 Proteins) to PS1 ratio.
Alzheimer's disease-causing proline substitutions lead to presenilin 1 aggregation and malfunction.
SLC2A13 is a novel gamma-secretase associated protein that regulates amyloid beta production without affecting Notch (show NOTCH1 Proteins) cleavage.
PS1 may affect neuroprotection and Alzheimer disease by controlling survival signaling of neuronal EGFR (show EGFR Proteins).
gamma-Secretase and presenilin mediate cleavage and phosphorylation of vascular endothelial growth factor receptor-1 (show FLT1 Proteins)
Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1\; PSEN2) or in the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (main component of amyloid deposits found in AD brains). Presenilins are postulated to regulate APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is thought that the presenilins are involved in the cleavage of the Notch receptor, such that they either directly regulate gamma-secretase activity or themselves are protease enzymes. Several alternatively spliced transcript variants encoding different isoforms have been identified for this gene, the full-length nature of only some have been determined.
, presenilin 1 (Alzheimer disease 3)
, presenilin-1 isoform I-463
, presenilin-1 isoform I-467
, presenilin 1
, presenilin alpha