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Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
Published on: March 16, 2016
Linking cognition to age and amyloid-β burden in the brain of a nonhuman primate (Microcebus murinus)
Daniel Schmidtke1, Elke Zimmermann1, Stéphanie G Trouche2
1Institute of Zoology, University of Veterinary Medicine Hannover, Hannover, Germany; Center for Systems Neuroscience Hannover, Hannover, Germany.
Abstract:
The gray mouse lemur (Microcebus murinus) is a valuable model in research on age-related proteopathies. This nonhuman primate, comparable to humans, naturally develops tau and amyloid-β proteopathies during aging. Whether these are linked to cognitive alterations is unknown. Here, standardized cognitive testing in pairwise discrimination and reversal learning in a sample of 37 aged (>5 years) subjects was combined with tau and amyloid-β histochemistry in individuals that died naturally. Correlation analyses in successfully tested subjects (n = 22) revealed a significant relation between object discrimination learning and age, strongly influenced by outliers, suggesting pathological cases. Where neuroimmunohistochemistry was possible, as subjects deceased, the naturally developed cortical amyloid-β burden was significantly linked to pretraining success (intraneuronal accumulations) and discrimination learning (extracellular deposits), showing that cognitive (pairwise discrimination) performance in old age predicts the natural accumulation of amyloid-β at death. This is the first description of a direct relation between the cortical amyloid-β burden and cognition in a nonhuman primate.
Insights
Gray mouse lemurs naturally develop brain changes like Alzheimer's disease. Aged lemurs with cognitive decline showed more amyloid-beta buildup in their brains, linking brain pathology to cognitive function.
Area of Science:
- Neuroscience
- Primate Research
- Aging Studies
Background:
- Gray mouse lemurs (Microcebus murinus) are valuable models for studying age-related diseases.
- They naturally develop tau and amyloid-beta proteopathies, similar to human aging.
- The link between these proteopathies and cognitive decline in this species is not well understood.
Purpose of the Study:
- To investigate the relationship between age-related proteopathies (tau and amyloid-beta) and cognitive function in aged gray mouse lemurs.
- To determine if naturally occurring amyloid-beta burden correlates with cognitive performance in this nonhuman primate model.
Main Methods:
- Standardized cognitive testing (pairwise discrimination, reversal learning) was performed on 37 aged gray mouse lemurs (>5 years).
- Tau and amyloid-beta levels were assessed using neurohistochemistry in deceased subjects.
- Correlation analyses were conducted to link cognitive performance with proteopathy markers.
Main Results:
- Cognitive performance in object discrimination learning was significantly related to age, with outliers suggesting pathological influence.
- Cortical amyloid-beta burden in deceased subjects was significantly linked to pretraining success and discrimination learning.
- This study establishes a direct correlation between cognitive performance and amyloid-beta accumulation in aged nonhuman primates.
Conclusions:
- Cognitive performance in aged gray mouse lemurs predicts the natural accumulation of cortical amyloid-beta.
- This research provides the first direct evidence linking amyloid-beta burden to cognition in a nonhuman primate model of aging.
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