Stimulation of amyloid precursor protein synthesis by adrenergic receptors coupled to cAMP formation.
Characterization of neurotrophic factors produced by immortalized mouse brain glial cells (VR-2g).
Amyloid beta-protein and lipid rafts: focused on biogenesis and catabolism.
Nardilysin prevents amyloid plaque formation by enhancing alpha-secretase activity in an Alzheimer's disease mouse model
Disease-Associated Mutations of TDP-43 Promote Turnover of the Protein Through the Proteasomal Pathway
Statins Reduce Amyloid beta-Peptide Production by Modulating Amyloid Precursor Protein Maturation and Phosphorylation Through a Cholesterol-Independent Mechanism in Cultured Neurons
Reduction of beta-Amyloid Accumulation by Reticulon 3 in Transgenic Mice
Potential repurposing of oncology drugs for the treatment of Alzheimer's disease
Neuronal beta-amyloid generation is independent of lipid raft association of beta-secretase BACE1: analysis with a palmitoylation-deficient mutant.
Chronic Cladribine Administration Increases Amyloid Beta Peptide Generation and Plaque Burden in Mice
Autoreactive-A beta antibodies promote APP beta-secretase processing
Abnormal cross-talk between mutant presenilin 1 (I143T, G384A) and glycosphingolipid biosynthesis
ER-stress-inducible Herp, facilitates the degradation of immature nicastrin
Oxidative Stress Up-Regulates Presenilin 1 in Lipid Rafts in Neuronal Cells
MEK inhibitors suppress beta-amyloid production by altering the level of a beta-C-terminal fragment of amyloid precursor protein in neuronal cells
Human CRB2 Inhibits gamma-Secretase Cleavage of Amyloid Precursor Protein by Binding to the Presenilin Complex
The Two-Hydrophobic Domain Tertiary Structure of Reticulon Proteins Is Critical for Modulation of beta-Secretase BACE1
Prostaglandin E(2) Stimulates the Production of Amyloid-beta Peptides through Internalization of the EP(4) Receptor
IGF-1 promotes beta-amyloid production by a secretase-independent mechanism
Expression of reticulon 3 in Alzheimer's disease brain
An E3 ubiquitin ligase, Synoviolin, is involved in the degradation of immature nicastrin, and regulates the production of amyloid beta-protein
A family of membrane proteins associated with presenilin expression and gamma-secretase function
Involvement of prostaglandin E-2 in production of amyloid-beta peptides both in vitro and in vivo
Endoplasmic reticulum chaperones inhibit the production of amyloid-beta peptides
A novel monoclonal antibody specific for the amino-truncated beta-amyloid A beta 5-40/42 produced from caspase-cleaved amyloid precursor protein
Reticulons RTN3 and RTN4-B/C interact with BACE1 and inhibit its ability to produce amyloid beta-protein
Reconstitution of gamma-secretase by truncated presenilin (PS) fragments revealed that PSC-terminal transmembrane domain is critical for formation of gamma-secretase complex
Characterization of APH-1 mutants with a disrupted transmembrane GxxxG motif
Altered localization of amyloid precursor protein under endoplasmic reticulum stress
Identification and characterization of a novel human APH-1b splice variant lacking exon 4
Homocysteic acid induces intraneuronal accumulation of neurotoxic A beta 42: Implications for the pathogenesis of Alzheimer's disease
Extracellular release of BACE1 holoproteins from human neuronal cells
Expression profiles of two human APH-1 genes and their roles in formation of presenilin complexes
Amyloid beta peptide binds a novel death-inducing protein, AB-DIP
Abnormal intracellular trafficking of high affinity nerve growth factor receptor, Trk, in stable transfectants expressing presenilin 1 protein
Glypican-1 as an A beta binding HSPG in the human brain: Its localization in DIG domains and possible roles in the pathogenesis of Alzheimer's disease
Enhanced generation of intracellular A beta 42 amyloid peptide by mutation of presenilins PS1 and PS2
Amino-truncated amyloid beta-peptide (A beta 5-40/42) produced from caspase-cleaved amyloid precursor protein is deposited in Alzheimer's disease brain
A novel mutation at position +11 in the intron following exon 10 of the tau gene in FTDP-17.
Pro-apoptotic effect of presenilin 2 (PS2) overexpression is associated with down-regulation of Bcl-2 in cultured neurons
Familial frontotemporal dementia and Parkinsonism with a novel mutation at an intron 10+11-splice site in the tau gene
Apoptotic neurons in Alzheimer's disease frequently show intracellular A beta 42 labeling
Overexpression of presenilin-2 enhances apoptotic death of cultured cortical neurons
Mutational analysis of intrinsic regions of presenilin 2 that determine its endoproteolytic cleavage and pathological function.
Transgenic mice with Alzheimer presenilin 1 mutations show accelerated neurodegeneration without amyloid plaque formation.
Increased expression of amyloid precursor protein and amyloid precursor-like protein 2 during trophic factor withdrawal-induced death of neuronal PC12 cells
How is membrane phospholipid biosynthesis controlled in neural tissues?
Control of membrane phosphatidylcholine biosynthesis by diacylglycerol levels in neuronal cells undergoing neurite outgrowth.
Secretion kinetics of Alzheimer's amyloid beta-protein differs from secreted beta-amyloid precursor protein.
THE DECREMENT OF MUSCARINIC RECEPTOR-MEDIATED CALCIUM INFLUX BY OVEREXPRESSION OF APP IN A MOUSE CHOLINERGIC CELL-LINE
Demonstration of amyloid beta-protein secretion in a mouse neuronal cell line.
Immortalization of fetal mouse brain glial cells by human papillomavirus type 16 E7 genes.
Trophic effect of beta-amyloid precursor protein on cerebral cortical neurons in culture.
Separation of protease activity from acetylcholinesterase of the electric EEL
Presence of calpain II immunoreactivity in senile plaques in Alzheimer's disease.
Familial hypobetalipoproteinaemia complicated by cerebellar ataxia and steatocystoma multiplex.
Aberrant accumulation of phospholipase C-delta in Alzheimer brains.
SUBCELLULAR-DISTRIBUTION OF ACETYLCHOLINESTERASE IN ALZHEIMERS-DISEASE - ABNORMAL LOCALIZATION AND SOLUBILIZATION
[Two sisters with pseudoidiopathic hypoparathyroidism presenting extensive intracranial calcification].