Pathological mechanism

Data

Name Post-synaptic Drebrin correlated with Alzheimer's cognitive decline

Description

Hypothesis Dendritic Spine Hypothesis Show Other

Extracelular pathological element

Intracelular pathological element Drebrin Show Other

Pathological action Is Correlated with Show Other

Process Cognitive Decline in Alzheimer's Show Other

Process action

Transmitter(s)

Receptor(s)

Channel(s)

Pharmacological Agent

Pharmacological Action

Brain region Hippocampus CA1 Show Other

Neuron Hippocampus CA1 pyramidal GLU cell Show Other

Cell model

Cellular compartment

PubMed ID 17379343

Citation

AlzWeb

Notes Kojima, N., & Shirao, T. (2007). Synaptic dysfunction and disruption of postsynaptic drebrin-actin complex: A study of neurological disorders accompanied by cognitive deficits. Neuroscience Research, 58(1), 1-5. The level of postsynaptic drebrin, a major F-actin-binding protein in dendritic spines, correlates well with the severity of cognitive impairment. We propose that an imbalanced regulation of the actin-regulatory machinery (loss of drebrin and increase of dephosphorylated cofilin) results in synaptic dysfunction, which underlies the cognitive impairment accompanying neurological disorders and normal aging.

Pathology Alzheimer Show Other

Stage Early Show Other

Question Exclude - biochemistry

Claim