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Abstract
Recent reports on experimental models of neurodegeneration in mice have strengthened the notion that environmental enrichment (EE) is beneficial, in terms of delayed onset and progression, to a variety of neurodegenerative diseases. These studies also revealed interesting mechanistic understandings as to how EE might function. While it is generally assumed that EE elicits transcriptional and translational events that on the whole tend to be neuroprotective and neurogenic, fairly specific changes that appear to target the underlying pathological causes of disease in these various mouse models have been noted. These include a possible restoration of brain-derived neurotrophic factor striatal transport in the R6/1 Huntington's mice and an elevation in the levels of amyloid-degrading enzyme neprilysin in the APPswe/PS1ΔE9 Alzheimic mice. An elevation in glial-derived neurotrophic factor coupled to a reduction in dopamine transporter may underlie beneficial effects in mice with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinsonian symptoms. How all these findings would translate to disease settings in human patients are unclear, but they do provide useful leads for further clinical and paraclinical investigations. © 2005 Elsevier Inc. All rights reserved.
Keywords
Alzheimer's disease, Environmental enrichment, Huntington's disease, Parkinson's disease
Source Title
Biochemical and Biophysical Research Communications
Publisher
Series/Report No.
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Date
2005
DOI
10.1016/j.bbrc.2005.05.162
Type
Review