Pathological mechanism

Data

Name p35/Cdk5 pathway mediates soluble amyloid-beta peptide-induced tau phosphorylation in vitro

Description

Hypothesis Dendritic Hypothesis - Ca++ currents Show Other

Extracelular pathological element Beta-amyloid (1-42) Show Other

Intracelular pathological element Tau protein Show Other

Pathological action Increases Show Other

Process Tau hyperphosphorylation Show Other

Process action Activates Show Other

Transmitter(s)

Receptor(s)

Channel(s) I L high threshold Show Other

Pharmacological Agent Calpain Inhibitor I Show Other P35 Antisense Oligonucleotides Show Other Verapamil Show Other

Pharmacological Action Blocks Show Other

Brain region

Neuron

Cell model

Cellular compartment

PubMed ID 12125077

Citation p35/Cdk5 pathway mediates soluble amyloid-beta peptide-induced tau phosphorylation in vitro. Show Other

AlzWeb

Notes "p35/Cdk5 pathway mediates soluble amyloid-beta peptide-induced tau phosphorylation in vitro. ... Results show that sAbeta(1-42) at relatively low levels (1-5 microM) dose-dependently increases tau phosphorylation at AD-specific phosphoepitopes in differentiated N2a/p35 cells compared with controls, an effect that is blocked by antisense oligonucleotides against p35. sAbeta(1-42)-induced tau phosphorylation is concomitant with an increase in both p25 to p35 ratio and Cdk5 activity (but not protein levels). Additionally, blockade of L-type calcium channels or inhibition of calpain completely abolishes this effect." (Town et al. 2002)

Pathology Alzheimer Show Other

Stage

Question

Claim Aß causes increased Ca++ influx by activation of L-type Ca++ channels Show Other