The beta A4-amyloid protein precursor (APP), the source of the beta A4-amyloid deposits found in Alzheimer brains, constitutes a family of transmembrane glycoproteins generated by alternative splicing. While exon 7 and exon 8 are well known to be alternatively spliced, APP mRNA isoforms without exon 15 were only recently identified in leukocytes and rat brain microglial cells and therefore deno...

It is widely accepted that amyloid β (Aβ) generated from amyloid precursor protein (APP) oligomerizes and fibrillizes to form neuritic plaques in Alzheimer's disease (AD), yet little is known about the contribution of APP to intracellular signaling events preceding AD pathogenesis. The data presented here demonstrate that APP expression and neuronal exposure to oligomeric Aβ42 enhance Ras/ERK s...

The Amyloid Precursor Protein (APP) is an integral membrane glycoprotein whose cleavage products, particularly Amyloid-β, accumulate in Alzheimer’s Disease (AD). APP is present at synapses and is thought to play a role in both the formation and plasticity of these critical neuronal structures. Despite the central role suggested for APP in AD pathogenesis, the mechanisms regulating APP in neuron...

Since its conception, smart app market has grown exponentially. Success in the app market depends on many factors among which the quality of the app is a significant contributor, such as energy use. Nevertheless, smartphones, as a subset of mobile computing devices. inherit the limited power resource constraint. Therefore, there is a challenge of maintaining the resource while increasing the ta...

Amyloid precursor proteins (APPs) are expressed in multiple organs and cell types in diverse species. Their conservation across species and high abundance in brain and the association of various APP missense mutations with autosomal dominant forms of familial Alzheimer's disease (FAD) suggest important roles for APP in the central nervous system. However, the basic functions of APP in the centr...

Mint adaptor proteins bind to the membrane-bound amyloid precursor protein (APP) and affect the production of pathogenic amyloid-β (Aβ) peptides related to Alzheimer's disease (AD). Previous studies have shown that loss of each of the three Mint proteins delays the age-dependent production of amyloid plaques in transgenic mouse models of AD. However, the cellular and molecular mechanisms underl...

Neuronal activity has an impact on beta cleavage of amyloid precursor protein (APP) by BACE1 to generate amyloid-beta peptide (Abeta). However, the molecular mechanisms underlying this effect remain to be elucidated. Cholesterol dependency of beta cleavage prompted us to analyze immunoisolated APP-containing detergent-resistant membranes from rodent brains. We found syntaxin 1 as a key molecule...

Platform desertion, or a developer’s stopping the development of an app for a platform, is a widespread phenomenon to the detriment of platforms. However, the extant literature focuses primarily on why app developers join—not leave—a platform. This app-level study develops two ideas: (a) coordination costs borne by an app’s developer are associated with platform desertion, and (b) these costs a...

The amyloid precursor protein (APP) was discovered in the 1980s as the precursor protein of the amyloid A4 peptide. The amyloid A4 peptide, also known as A-beta (Aβ), is the main constituent of senile plaques implicated in Alzheimer's disease (AD). In association with the amyloid deposits, increasing impairments in learning and memory as well as the degeneration of neurons especially in the hip...

The intracellular transport and localization of amyloid precursor protein (APP) are critical determinants of APP processing and β-amyloid peptide production, thus crucially important for the pathophysiology of Alzheimer's disease (AD). Notably, the C-terminal Y682ENPTY687 domain of APP binds to specific adaptors controlling APP trafficking and sorting in neurons. Mutation on the Y682 residue to...