Pathological mechanism

Data

Name Abeta inhibits late LTP in animal models of Alzheimers

Description

Hypothesis LTP hypothesis Show Other

Extracelular pathological element beta Amyloid Show Other

Intracelular pathological element

Pathological action Inhibits Show Other

Process LTP Show Other

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 12740129

Citation Alterations in synaptic transmission and long-term potentiation in hippocampal slices from young and aged PDAPP mice. Show Other Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins. Show Other Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain. Show Other Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice. Show Other In vivo synaptic transmission in young and aged amyloid precursor protein transgenic mice. Show Other Neuronal deficiency of presenilin 1 inhibits amyloid plaque formation and corrects hippocampal long-term potentiation but not a cognitive defect of amyloid precursor protein [V717I] transgenic mice. Show Other Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models. Show Other Similar levels of long-term potentiation in amyloid precursor protein -null and wild-type mice in the CA1 region of picrotoxin treated slices. Show Other Soluble oligomers of beta amyloid (1-42) inhibit long-term potentiation but not long-term depression in rat dentate gyrus. Show Other Synaptic plasticity in animal models of early Alzheimer's disease. Show Other

AlzWeb

Notes Transgenic mice Alzhiemers models and hippocampal slice preparations from wild type rats support the Abeta Alzheimers hypothesis: that Abeta is a primary cause of Alzheimers (reviewed in Rowan et al 2003). Various transgenic mice show inhibition in LTP before amyloid plaques are deposited (Larson et al. 1999, Giacchino et al. 2000, Hsia et al. 1999, Chapman et al. 1999, Fitzjohn et al.2000, Moechars et al. 1999,Dewachter et al. 2002). Normal rat electrophysiology in hippocampal slices show that soluble 500 nM Abeta inhibits LTP induction (Lambert et al. 1998, Wang et al. 2002). These findings support the hypothesis that soluble Abeta disrupts synaptic plasticity in the hippocampus in early Alzheimers before Abeta plaques form.

Pathology Alzheimer Show Other

Stage Early Show Other

Question

Claim