Satoshi Tsubuki
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View article: The Role of Neprilysin and Insulin-Degrading Enzyme in the Etiology of Sporadic Alzheimer's Disease
The Role of Neprilysin and Insulin-Degrading Enzyme in the Etiology of Sporadic Alzheimer's Disease Open
An age-dependent decline in the amyloid-β (Aβ)-degrading enzyme neprilysin (NEP) has been implicated in the pathogenesis of sporadic Alzheimer's disease (AD). Recently identified risk alleles in the NEP-coding gene further support its role…
View article: Metabolic resistance of Aβ3pE-42, a target epitope of the anti-Alzheimer therapeutic antibody, donanemab
Metabolic resistance of Aβ3pE-42, a target epitope of the anti-Alzheimer therapeutic antibody, donanemab Open
The amyloid β peptide (Aβ), starting with pyroglutamate (pE) at position 3 and ending at position 42 (Aβ3pE-42), predominantly accumulates in the brains of Alzheimer’s disease. Consistently, donanemab, a therapeutic antibody raised against…
View article: Metabolic resistance of Aβ3pE-42, target epitope of the anti-Alzheimer therapeutic antibody, donanemab
Metabolic resistance of Aβ3pE-42, target epitope of the anti-Alzheimer therapeutic antibody, donanemab Open
The amyloid β peptide (Aβ) starting with pyroglutamate (pE) at position 3 and ending at position 42 (Aβ3pE-42) is a dominant species that accumulates in the Alzheimer’s disease (AD) brain. Consistently, a therapeutic antibody raised agains…
View article: Recent Advances in the Modeling of Alzheimer’s Disease
Recent Advances in the Modeling of Alzheimer’s Disease Open
Since 1995, more than 100 transgenic (Tg) mouse models of Alzheimer’s disease (AD) have been generated in which mutant amyloid precursor protein (APP) or APP/presenilin 1 (PS1) cDNA is overexpressed ( 1st generation models ). Although many…
View article: Somatostatin-evoked Aβ catabolism in the brain: Mechanistic involvement of α-endosulfine-KATP channel pathway
Somatostatin-evoked Aβ catabolism in the brain: Mechanistic involvement of α-endosulfine-KATP channel pathway Open
Alzheimer’s disease (AD) is characterized by the deposition of amyloid β peptide (Aβ) in the brain. The neuropeptide somatostatin (SST) regulates Aβ catabolism by enhancing neprilysin (NEP)-catalyzed proteolytic degradation. However, the m…
View article: Neprilysin-sensitive amyloidogenic Aβ versus IDE-sensitive soluble Aβ: a probable mechanistic cause for sporadic Alzheimer’s disease
Neprilysin-sensitive amyloidogenic Aβ versus IDE-sensitive soluble Aβ: a probable mechanistic cause for sporadic Alzheimer’s disease Open
Neprilysin (NEP) and insulin-degrading enzyme (IDE) are considered the two major catabolic enzymes that degrade amyloid β peptide (Aβ), the primary cause of Alzheimer’s disease (AD). However, their roles in Aβ metabolism in vivo have never…
View article: α-Endosulfine regulates amyloid β 42 via the modulation of neprilysin activity
α-Endosulfine regulates amyloid β 42 via the modulation of neprilysin activity Open
The neuropeptide somatostatin (SST) regulates amyloid β peptide (Aβ) catabolism by enhancing neprilysin (NEP)-catalyzed proteolytic degradation. However, the mechanism by which SST regulates NEP activity remains unclear. Here we report the…
View article: Somatostatin receptor subtypes 1 and 4 redundantly regulate neprilysin, the major amyloid-beta degrading enzyme in brain
Somatostatin receptor subtypes 1 and 4 redundantly regulate neprilysin, the major amyloid-beta degrading enzyme in brain Open
Alzheimer’s disease (AD) brains are characterized by increased levels of the pathogenic amyloid beta (Aβ) peptide, which accumulates into extracellular plaques. Finding a way to lower Aβ levels is fundamental for the prevention and treatme…