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Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration.

Abstract：

:Degeneration of basal forebrain cholinergic neurons (BFCNs) contributes to cognitive dysfunction in Alzheimer's disease (AD) and Down's syndrome (DS). We used Ts65Dn and Ts1Cje mouse models of DS to show that the increased dose of the amyloid precursor protein gene, App, acts to markedly decrease NGF retrograde transport and cause degeneration of BFCNs. NGF transport was also decreased in mice expressing wild-type human APP or a familial AD-linked mutant APP; while significant, the decreases were less marked and there was no evident degeneration of BFCNs. Because of evidence suggesting that the NGF transport defect was intra-axonal, we explored within cholinergic axons the status of early endosomes (EEs). NGF-containing EEs were enlarged in Ts65Dn mice and their App content was increased. Our study thus provides evidence for a pathogenic mechanism for DS in which increased expression of App, in the context of trisomy, causes abnormal transport of NGF and cholinergic neurodegeneration.

journal_name

Neuron

journal_title

Neuron

authors

Salehi A,Delcroix JD,Belichenko PV,Zhan K,Wu C,Valletta JS,Takimoto-Kimura R,Kleschevnikov AM,Sambamurti K,Chung PP,Xia W,Villar A,Campbell WA,Kulnane LS,Nixon RA,Lamb BT,Epstein CJ,Stokin GB,Goldstein LS,Mobley WC

doi

10.1016/j.neuron.2006.05.022

subject

Has Abstract

pub_date

2006-07-06 00:00:00

pages

29-42

issue

1

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(06)00414-4

journal_volume

51

pub_type

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