Creatine therapy provides neuroprotection after onset of clinical symptoms in Huntington's disease transgenic mice
Open accessAbstract
While there have been enormous strides in the understanding of Huntington's disease (HD) pathogenesis, treatment to slow or prevent disease progression remains elusive. We previously reported that dietary creatine supplementation significantly improves the clinical and neuropathological phenotype in transgenic HD mice lines starting at weaning, before clinical symptoms appear. We now report that creatine administration started after onset of clinical symptoms significantly extends survival in the R6/2 transgenic mouse model of HD. Creatine treatment started at 6, 8, and 10 weeks of age, analogous to early, middle, and late stages of human HD, significantly extended survival at both the 6‐ and 8‐week starting points. Significantly improved motor performance was present in both the 6‐ and 8‐week treatment paradigms, while reduced body weight loss was only observed in creatine‐supplemented R6/2 mice started at 6 weeks. Neuropathological sequelae of gross brain and neuronal atrophy and huntingtin aggregates were delayed in creatine‐treated R6/2 mice started at 6 weeks. We show significantly reduced brain levels of both creatine and ATP in R6/2 mice, consistent with a bioenergetic defect. Oral creatine supplementation significantly increased brain concentrations of creatine and ATP to wild‐type control levels, exerting a neuroprotective effect. These findings have important therapeutic implications, suggesting that creatine therapy initiated after diagnosis may provide significant clinical benefits to HD patients.
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Creatine significantly improves survival, improves motor performance, slows the development of brain atrophy, increases brain ATP levels, delays atrophy of striatal neurons and the formation of Htt-positive aggregates in the R6/2 and N-171-82Q transgenic mouse models of HD.
“We found that creatine significantly improves survival, improves motor performance, slows the development of brain atrophy, increases brain ATP levels, delays atrophy of striatal neurons and the formation of Htt-positive aggregates in the R6/2 and N-171-82Q transgenic mouse models of HD118-120.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [119]
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- Authors
- Dedeoglu, A., Kubilus, J. K., Yang, L., Ferrante, K. L., Hersch, S. M., Beal, M. F., & Ferrante, A. R. J.
- Affiliations
- Boston University (US)
- NewYork–Presbyterian Hospital (US)
- Massachusetts General Hospital (US)
- Harvard University (US)
- Corresponding author
- Ferrante, And Robert J.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2003-04-23
- Volume
- 85
- Issue
- 6
- Pages
- 1359-1367
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- PMC
- PMC2866522
- OpenAlex
- W1797863618
- Cited by
- 169
- References
- 47
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 4 · 2020: 1 · 2019: 5 · 2018: 5 · 2017: 4 · 2016: 10 · 2015: 3 · 2014: 13 · 2013: 6 · 2012: 9
- FWCI
- 4.74
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5r29ns037102-02)
- National Institute on Aging (AG 12992, AG 13846, P01AG014930, P30AG013846, P01AG012992, AG14930)
- National Institute of Neurological Disorders and Stroke (NS 39258, NS37102, NS 35255, NS38180, R01NS035255, R01NS039258)
- National Center for Complementary and Integrative Health (AT00613, R01AT000613, U01AT000613)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Metabolism and Genetic Disorders
- Keywords
- Huntington's disease, creatine supplementation, neuroprotection, R6/2 transgenic mice, treatment initiation timing, survival extension, motor performance, huntingtin aggregates, neuronal atrophy, brain energy metabolism, ATP levels, weight loss
- MeSH terms
- Adenosine Triphosphate, Administration, Oral, Animals, Body Weight, Brain, Corpus Striatum, Creatine, Disease Models, Animal, Huntington Disease, Mice, Transgenic, Motor Activity, Survival Rate, Treatment Outcome, Neostriatum, Disease Progression, Mice
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