Prolonged running, not fluoxetine treatment, increases neurogenesis, but does not alter neuropathology, in the 3xTg mouse model of Alzheimer’s disease
Open accessAbstract
Reductions in adult neurogenesis have been documented in the original 3xTg mouse model of Alzheimer's disease (AD), notably occurring at the same age when spatial memory deficits and amyloid plaque pathology appeared. As this suggested reduced neurogenesis was associated with behavioral deficits, we tested whether activity and pharmacological stimulation could prevent memory deficits and modify neurogenesis and/or neuropathology in the 3xTg model backcrossed to the C57Bl/6 strain. We chronically administered the antidepressant fluoxetine to one group of mice, allowed access to a running wheel in another, and combined both treatments in a third cohort. All treatments lasted for 11 months. The female 3xTg mice failed to exhibit any deficits in spatial learning and memory as measured in the Morris water maze, indicating that when backcrossed to the C57Bl/6 strain, the 3xTg mice lost the behavioral phenotype that was present in the original 3xTg mouse maintained on a hybrid background. Despite this, the backcrossed 3xTg mice expressed prominent intraneuronal amyloid beta (Aβ) levels in the cortex and amygdala, with lower levels in the CA1 area of the hippocampus. In the combined cohort, fluoxetine treatment interfered with exercise and reduced the total distance run. The extent of Aβ neuropathology, the tau accumulations, or BDNF levels, were not altered by prolonged exercise. Thus, neuropathology was present but not paralleled by spatial memory deficits in the backcrossed 3xTg mouse model of AD. Prolonged exercise for 11 months did improve the long-term survival of newborn neurons generated during middle-age, whereas fluoxetine had no effect. We further review and discuss the relevant literature in this respect.
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Negative results of chronic administration were reported and neurogenesis-independent mechanisms of fluoxetine action were described.
“Negative results of chronic administration were reported (Marlatt et al., 2013) and neurogenesis-independent mechanisms of fluoxetine action were described (David et al., 2009).”
From Serotonin and neuroplasticity – Links between molecular, functional and structural pathophysiology in depression (2017) · cites this paper as Marlatt et al., 2013
Prolonged running in the 3xTg AD mouse model increased neurogenesis (in terms of progenitor cells survival) without effects on differentiation and no evident influence on the AD pathology.
“Concerning voluntary exercise, for example it has been shown that prolonged running in the 3xTg AD mouse model did increase neurogenesis (in terms of progenitor cells survival) without effects on differentiation and no evident influence on the AD pathology (Marlatt et al., 2013).”
From Depression and adult neurogenesis: Positive effects of the antidepressant fluoxetine and of physical exercise (2018) · cites this paper as Marlatt et al., 2013
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- Authors
- Marlatt, M. W., Potter, M. C., Bayer, T. A., van Praag, H., & Lucassen, P. J.
- Affiliations
- National Institute on Aging (US)
- University of Göttingen (DE)
- University of Amsterdam (NL)
- Corresponding author
- Lucassen, Paul J.
- Venue
- Current Topics in Behavioral Neurosciences
- Publisher
- Springer Berlin Heidelberg
- Published
- 2013
- Volume
- 15
- Pages
- 313-340
- ISSN
- 1866-3370 (ISSN-L)
- 1866-3389
- PMC
- PMC4554490
- OpenAlex
- W2096481146
- Cited by
- 92
- References
- 71
- Citations by year
- 2026: 2 · 2024: 7 · 2023: 1 · 2022: 2 · 2021: 6 · 2020: 7 · 2019: 11 · 2018: 8 · 2017: 14 · 2016: 11 · 2015: 9 · 2014: 12 · 2013: 2
- FWCI
- 43.59
- Type
- book chapter
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Current topics in behavioral neurosciences (publishedVersion)
- PubMed (publishedVersion)
- UvA-DARE (University of Amsterdam) (publishedVersion)
- PubMed Central (acceptedVersion)
- UvA-DARE (University of Amsterdam) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek
- National Institutes of Health
- National Institute on Aging (ZIAAG000328, Z01AG000328)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, 3xTg mouse model, adult neurogenesis, physical activity, running wheel, fluoxetine, antidepressant treatment, spatial memory impairment, amyloid-beta, tau accumulation, brain-derived neurotrophic factor, hippocampus, neuropathology, behavioral phenotypes
- MeSH terms
- Alzheimer Disease, Amygdala, Animals, Behavior, Animal, Cerebral Cortex, Combined Modality Therapy, Disease Models, Animal, Exercise Therapy, Female, Fluoxetine, Hippocampus, Learning, Memory, Mice, Inbred C57BL, Mice, Transgenic, Running, Selective Serotonin Reuptake Inhibitors, Maze Learning, Mice, Cerebrum, Neurogenesis
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