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." (Dedeoglu, et al., 2003) Specifically it is stated that the "...Neuropathological sequelae of gross brain and neuronal atrophy and huntington 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." (Dedeoglu, et al., 2003)
VII. Ferrante et al. (2002)
The work of Ferrante et al. (2002) entitled: 'Therapeutic Effects of Coenzyme Q10 and Remacemide in Transgenic Mouse Models of Huntington's Disease" states that there is "...substantial evidence that bioenergetic defects and excitotoxicity may play a role in the pathogenesis of Huntington's disease (HD). Potential therapeutic strategies for neurodegenerative diseases in which there is reduced energy metabolism and NMDA-mediated excitotoxicity are the administration of the mitochondrial cofactor coenzyme Q10 and the NMDA antagonist remacemide." (2003) Ferrante et al. states that they found "...that oral administration of either coenzyme Q10 or remacemide significantly extended survival and delayed the development of motor deficits, weight loss, cerebral atrophy, and neuronal intranuclear inclusions in the R6/2 transgenic mouse model of HD. The combined treatment, using coenzyme Q10 and remacemide together, was more efficacious than either compound alone, resulting in an approximately 32 and 17% increase in survival in the R6/2 and N171-82Q mice, respectively." (Ferrante et al., 2003) This study reports that magnetic resonance imaging "...showed that combined treatment significantly attenuated ventricular enlargement in vivo. These studies further implicate defective energy metabolism and excitotoxicity in the R6/2 and N171-82Q transgenic mouse models of HD and are of interest in comparison with the outcome of a recent clinical trial examining coenzyme Q10 and remacemide in HD patients." (Ferrante et al., 2003)
VIII. Aziz et al. (2008)
The work of Aziz, et al. (2008) entitled: "Weight Loss in Huntington Disease Increases with Higher CAG Repeat Number" states that Huntington Disease (HD) is a hereditary neurogenerative disorder "...caused by an expanded number of CAG repeats in the huntingtin gene. A hallmark of HD is unintended weight loss, the cause of which is unknown." Aziz et al. reports that in order to understand the mechanisms underlying weight loss in Huntington's Disease, they studied "its relation to other disease characteristics including motor, cognitive, and behavioral disturbances and CAG repeat number." (2008) the study involved 517 patients in the early stages of Huntington's Disease and "applied mixed-effects model analyses to correlate weight changes over 3 years to CAG repeat number and various components of the Unified Huntington's Disease Rating Scale (UHDRS)." (Aziz, et al., 2008) Additionally assessed was the "...relation between CAG repeat number and body weight and caloric intake in the R6/2 mouse model of HD." (Aziz, et al., 2008) Results of the study report: "In patients with HD, mean body mass index decreased with -0.15 units per year (p < 0.001). However, no single UHDRS component, including motor, cognitive, and behavioral scores, was independently associated with the rate of weight loss. Patients with HD with a higher CAG repeat number had a faster rate of weight loss. Similarly, R6/2 mice with a larger CAG repeat length had a lower body weight, whereas caloric intake increased with larger CAG repeat length." (Aziz, et al., 2008) Conclusions state that weight loss in Huntington's Disease "...is directly linked to CAG repeat length and is likely to result from a hypermetabolic state. Other signs and symptoms of HD are unlikely to contribute to weight loss in early disease stages. Elucidation...
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