Related Experiment Video

Updated: Aug 19, 2026

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
08:27

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Published on: March 11, 2020

Creatine supplementation lowers brain glutamate levels in Huntington's disease

Andreas Bender1, Dorothee P Auer, Thomas Merl

  • 1Department of Neurology, Klinikum Grosshadern, University of Munich, Marchioninistrasse 15, 81377 Munich, Germany.

Journal of Neurology
|January 27, 2005
PubMed

Insights

Creatine supplementation in Huntington's disease (HD) patients showed reduced brain glutamate levels, suggesting a potential therapeutic benefit. Further long-term clinical trials are needed to confirm these findings for neuroprotection in HD.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Clinical Neurology

Background:

  • In vitro and animal studies suggest creatine (Cr) may slow neurodegeneration in Huntington's disease (HD).
  • Previous clinical trials have not replicated these neuroprotective effects, potentially due to insufficient treatment duration.
  • Huntington's disease is characterized by neurodegeneration and impaired brain metabolism.

Purpose of the Study:

  • To evaluate the effect of oral creatine supplementation on brain metabolite levels in patients with Huntington's disease using proton magnetic resonance spectroscopy ((1)H-MRS).
  • To assess creatine's impact on surrogate markers of neurodegeneration in HD patients.

Main Methods:

  • Twenty patients with Huntington's disease received oral creatine supplementation for 8-10 weeks.
  • Proton magnetic resonance spectroscopy ((1)H-MRS) was used to measure brain metabolite levels in the parieto-occipital cortex before and after treatment.
  • Clinical assessments included the motor section of the Unified Huntington's Disease Rating Scale and the Mini Mental State Examination.

Main Results:

  • Oral creatine supplementation led to a significant decrease in cortical glutamate (Glu) and glutamate+glutamine (Glx) levels (p<0.001).
  • N-acetylaspartate showed a trend towards decrease (p=0.073), while other metabolites remained unchanged.
  • No significant improvements were observed in the clinical rating scales.

Conclusions:

  • The observed decrease in cortical Glx and Glu suggests creatine may enhance the Glu-Gln cycle, a pathway impaired in HD.
  • These metabolic changes indicate a potential therapeutic role for creatine in managing Huntington's disease.
  • Long-term clinical trials are warranted to validate creatine's efficacy and safety in HD patients.

More Related Videos

Treating SCA1 Mice with Water-Soluble Compounds to Non-Specifically Boost Mitochondrial Function11:47

Treating SCA1 Mice with Water-Soluble Compounds to Non-Specifically Boost Mitochondrial Function

Published on: January 22, 2017

Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models10:46

Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models

Published on: May 3, 2017

Related Concept Videos

Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show reduced penetrance,...
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function. They...
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of its...