Age exacerbates abnormal protein expression in a mouse model of Down syndrome.

Citation data:

Neurobiology of aging, ISSN: 1558-1497, Vol: 57, Page: 120-132

Publication Year:
2017
Usage 40
Abstract Views 40
Captures 6
Readers 6
Mentions 1
News Mentions 1
Social Media 2
Tweets 2
Citations 2
Citation Indexes 2
Repository URL:
https://mouseion.jax.org/stfb2017/131
PMID:
28641136
DOI:
10.1016/j.neurobiolaging.2017.05.002
Author(s):
Ahmed, Md Mahiuddin; Block, Aaron; Tong, Suhong; Davisson, Muriel T; Gardiner, Katheleen J
Publisher(s):
Elsevier BV; Pergamon Press
Tags:
Neuroscience; Biochemistry, Genetics and Molecular Biology; Medicine; Life Sciences; Medicine and Health Sciences
Most Recent Tweet View All Tweets
Most Recent News Mention
article description
The Ts65Dn is a popular mouse model of Down syndrome (DS). It displays DS-relevant features of learning/memory deficits and age-related loss of functional markers in basal forebrain cholinergic neurons. Here we describe protein expression abnormalities in brain regions of 12-month-old male Ts65Dn mice. We show that the magnitudes of abnormalities of human chromosome 21 and non-human chromosome 21 orthologous proteins are greater at 12 months than at ∼6 months. Age-related exacerbations involve the number of components affected in the mechanistic target of rapamycin pathway, the levels of components of the mitogen-activated protein kinase pathway, and proteins associated with Alzheimer's disease. Among brain regions, the number of abnormalities in cerebellum decreased while the number in cortex greatly increased with age. The Ts65Dn is being used in preclinical evaluations of drugs for cognition in DS. Most commonly, drug evaluations are tested in ∼4- to 6-month-old mice. Data on age-related changes in magnitude and specificity of protein perturbations can be used to understand the molecular basis of changes in cognitive ability and to predict potential age-related specificities in drug efficacies.