Researchers have disclosed the mechanism by which environmental stimulation decelerates Alzheimer's disease, further affirming that increased mental and physical activity //retards neurological decline.
A paper to this effect presented by Ambrée et al., "Reduction of amyloid angiopathy and A? plaque burden after enriched housing in TgCRND8 mice: involvement of multiple pathways," appears in the2006 August issue of The American Journal of Pathology.
Alzheimer's disease, the leading cause of senile dementia, presents with cognitive and behavioral deficiencies resulting in part from accumulation of amyloid? (A?) deposits within the brain (A? plaques) and its blood vessels (amyloid angiopathy). Although previous studies have shown that increased mental and physical activity can slow the progression of the disease, how such deceleration occurs has been unclear until now.
Dr. Kathy Keyvani's group at University Hospital Muenster examined the effects of environmental stimulation on the brain pathology of TgCRND8 mice. These mice, which express a mutant form of A? found in some Alzheimer's patients, develop Alzheimer-like features including A? plaques and cognitive deficits. To study the effects of enrichment, mice were housed in either standard cages or enriched cages, similar to the standard but with access to a stimulus cage containing permanent fixtures (rope and gnawing wood) as well as removable items (tunnels, balls, ladders, ramps, and exercise wheels) that were changed on a rotating basis.
Following five months of standard versus enriched housing, mouse brains were examined for signs of disease. Mice housed in the enriched environment had fewer A? plaques, smaller plaque size, and reduced amyloid angiopathy compared to mice housed in standard cages. Interestingly, there were no differences in the levels of soluble A? peptide or the transcriptional/translational expression levels of its precursor protein (APP) or the
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