Pathological mechanism

Data

Name Abeta oligomer inhibits p-21 activated kinase and stimulates ROCK signalling

Description

Hypothesis LTP hypothesis Show Other

Extracelular pathological element beta Amyloid Show Other

Intracelular pathological element p-21 activated kinase (PAK) Show Other

Pathological action Inhibits Show Other

Process

Process action

Transmitter(s)

Receptor(s)

Channel(s)

Pharmacological Agent

Pharmacological Action

Brain region Hippocampus CA1 Show Other

Neuron

Cell model

Cellular compartment

PubMed ID

Citation

AlzWeb

Notes Salminen, A., Suuronen, T., & Kaarniranta, K. (2008). ROCK, PAK, and toll of synapses in alzheimer's disease. Biochemical and Biophysical Research Communications, 2008 Jul 11;371(4):587-90. Brain tissue in AD recognizes the beta-amyloid peptide oligomers as foreign protein particles and mounts an inflammatory defense via Toll-like receptor (TLR) signaling which causes synaptic impairment. Synaptic dysfunction is a sensitive parameter of the AD pathology. Rho GTPases and the Rho kinases, ROCK1/2, and PAK1-3, are important regulators of synaptic plasticity, especially in maintaining the actin cytoskeleton of dendritic spines.

Pathology Alzheimer Show Other

Stage Late Show Other

Question Exclude - biochemistry

Claim