1.      A
study of Gelderblom et al showed the efficacy and safety of bupropion in the
treatment of apathy in Huntington’s disease. This is a multi-center,
randomized, double-blind, placebo-controlled, 2×2 crossover phase 2b
investigator-initiated trial (IIT). Genetically verified Huntington patients
aged 25 to 75 years were included in the trial. Patients received once daily
150 mg bupropion or placebo for 2 weeks, followed by 300 mg bupropion or
placebo per day for 8 weeks. The primary outcome parameter was a significant alteration
in the Apathy Evaluation Scale (AES) score after ten weeks of treatment as
judged by an informant (AES-I) living in close proximity with the study
participant. The secondary outcome parameters involves the changes of AES
scores determined by the patient (AES-S) or the clinical investigator (AES-C),
psychiatric symptoms (NPI (Neuropsychiatric Inventory), HADS-SIS (The Hospital
Anxiety and Depression Scale combined with the Snaith Irritability Scale),
UHDRS-Behaviour (Unified Huntington’s Disease Rating Scale)), cognitive
performance (SDMT (Symbol Digit Modalities Test),
Stroop, VFT (Verbal
fluency tests ), MMSE (Mini Mental Status Examination)),  motor symptoms (UHDRS-Motor), activities of
daily function (TFC (total functional capacity), UHDRS-Function), and caregiver
distress (NPI-D) (Gelderblom et al., 2017). Additionally, the author also
observed the effect of bupropion on brain structure as well as brain responses
and functional connectivity during reward processing in a gambling task using
magnetic resonance imaging (MRI). There were no significant treatment group
variation in the clinical primary and secondary outcome parameters. At
endpoint, there was no statistically significant difference between treatment
groups for all clinical primary and secondary outcome variables. Irrespective
of the intervention (bupropion or placebo), informants and clinical
investigators observed a significant improvement of the symptoms of apathy
(AES-I, AES-C) or the apathy syndrome (NPI-Apathy, UHDRS-Apathy) primarily during
the first treatment period. Notably, this was not observed in the AES-S scores.
Therefore, it is concluded that bupropion does not influence the severity of
apathy in non depressed Huntington disease patients as enumerated by the AES
and other behavioural assessment tools (Gelderblom et al., 2017).

2.      A
study of Steven et al demonstrated the efficacy of high doses of creatine for
slowing the progressive functional decline in patients with early symptoms of
Huntington’s disease. This was  a
multicenter, randomized, double-blind, placebo-controlled study of up to 40 g
daily of creatine monohydrate in participants with stage I and II HD treated
for up to 48 months. Eligible participants were in stage I or II of HD
(TFC?7),were ?18 years old, had a confirmatory family history or CAGn ?36, were
capable of providing informed consent and complying with procedures, and were
on stable doses of any concomitant psychotropic medications. Women of
childbearing potential could not be pregnant or lactating and were required to
use adequate contraception methods. Participants were excluded for screening
creatinine levels >2.0 mg/dL or other laboratory abnormalities suggesting
risk during the study. Exposure to investigational drugs, supplemental creatine
at doses >10 g daily or supplemental coenzyme Q10 at doses
>600 mg daily within 30 days of randomization, or unstable psychiatric or
medical illness were disallowed. The primary outcome measure was the rate of
change in total functional capacity (TFC) between baseline and end of
follow-up. Secondary outcome measures included changes in additional clinical
scores, tolerability, and quality of life. Safety was assessed by adverse
events and laboratory studies. The estimated rates of decline in the primary
outcome measure (TFC) were 0.82 points per year for participants on creatine,
0.70 points per year for participants on placebo, favoring placebo (nominal 95%
confidence limits 20.11 to 0.35). Adverse events, mainly gastrointestinal, were
significantly more common in participants on creatine. Serious adverse events,
including deaths, were more frequent in the placebo group. Additionally,
Subgroup analysis suggested that men and women may respond differently to
creatine treatment. Therefore, it concludes that there is no role of creatine
administration for delaying functional decline in early manifest huntington’s
disease.

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3.      A
Study of Mc Garry et al demonstrated that chronic treatment of early-stage
Huntington’s disease with high dose coenzyme Q10 (CoQ) will slow the
progressive functional decline of HD. A multicenter randomized, double-blind,
placebo-controlled trial was conducted. Patients with early-stage HD (n 5 609)
were enrolled at 48 sites randomized to receive either CoQ 2,400 mg/d or
matching placebo, then followed for 60 months. The primary outcome variable was
the change from baseline to month 60 in Total Functional Capacity score (for
patients who survived) combined with time to death (for patients who died)
analyzed using a joint-rank analysis approach. CoQ was generally safe and
well-tolerated throughout the study. The most common adverse event categories,
patients experiencing at least one event, were psychiatric disturbances,
infections, gastrointestinal disturbances, injury, and nervous system
disturbances. In this study, there were no beneficial effect of CoQ was
detected on the primary outcome variable, and the trial was concluded early on
the basis of an interim analysis for futility. None of the secondary outcome
variables demonstrated a beneficial effect of CoQ with the exception of the
Word reading score on the Stroop test, which as a lone finding may be spurious.
Therefore, it is concluded that the trial provides no evidence that CoQ slows
the progression of functional decline in HD, and these data do not justify use
of CoQ as a treatment in HD.

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