Pathological mechanism

Data

Name Co-localization of amyloid beta and tau in Alzheimer's disease synaptosomes.

Description

Hypothesis Dendritic Spine Hypothesis Show Other

Extracelular pathological element beta Amyloid Show Other

Intracelular pathological element Tau protein Show Other

Pathological action

Process Synapse Loss Show Other

Process action Co-localizes with Show Other

Transmitter(s)

Receptor(s)

Channel(s)

Pharmacological Agent

Pharmacological Action

Brain region

Neuron

Cell model Human Post-mortem Study Show Other

Cellular compartment

PubMed ID 18467692

Citation

AlzWeb

Notes Synaptic Abeta and p-tau fluorescence was significantly correlated (r = 0.683, P < 0.004), and dual-labeling experiments demonstrated that 24.1% of Abeta-positive terminals were also positive for p-tau, with the highest fraction of dual labeling (39.3%) in the earliest affected region, the entorhinal cortex in synaptosomes prepared from AD brains. Fein, J. A., Sokolow, S., Miller, C. A., Vinters, H. V., Yang, F., Cole, G. M., et al. (2008). Co-Localization of amyloid beta and tau pathology in alzheimer's disease synaptosomes. The American Journal of Pathology, 172(6), 1683-1692.

Pathology

Stage

Question Exclude - biochemistry

Claim