Related Experiment Video
Updated: Jul 13, 2026
08:27
Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
Published on: March 11, 2020
Is brain lactate increased in Huntington's disease?
W R Wayne Martin1, Marguerite Wieler, Christopher C Hanstock
1Division of Neurology, University of Alberta, Edmonton, Alberta, Canada. wayne.martin@ualberta.ca
Journal of the Neurological Sciences
|July 28, 2007
Summary
Huntington's disease (HD) patients show increased brain lactate, suggesting impaired energy metabolism. This study investigated cerebrospinal fluid (CSF) lactate's role in magnetic resonance spectroscopy (MRS) findings in HD.
Area of Science:
- Neuroscience
- Biochemistry
- Medical Imaging
Background:
- Impaired brain energy metabolism and increased lactate are implicated in Huntington's disease (HD) pathogenesis.
- Magnetic resonance spectroscopy (MRS) studies on HD metabolism have yielded conflicting results regarding lactate levels.
Purpose of the Study:
- To investigate the contribution of cerebrospinal fluid (CSF) lactate to MRS-detected metabolic changes in HD.
- To evaluate regional brain lactate levels in HD patients compared to controls using advanced MRS techniques.
Main Methods:
- Single voxel MRS at 3 Tesla was performed on 23 HD patients and 28 controls.
- MRS voxels were segmented into grey matter, white matter, and CSF.
- Regional lactate content was extrapolated to a hypothetical 100% brain voxel to control for CSF lactate variations.
Main Results:
- Significantly increased lactate/creatine and lactate/N-acetyl aspartate (Lac/NAA) ratios were observed in parieto-occipital and cerebellar regions of HD patients.
- Extrapolated Lac/NAA ratios in a theoretical 100% brain voxel were higher in HD patients, though not statistically significant.
- These findings suggest a potential, regionally non-specific increase in brain lactate in manifest HD.
Conclusions:
- Brain lactate content may be increased in manifest Huntington's disease, supporting impaired mitochondrial function and abnormal energy metabolism.
- The precise contribution of CSF lactate to observed MRS changes in HD requires further investigation.
- The study highlights potential metabolic alterations in HD, offering insights into disease mechanisms.
More Related Videos
09:26Functional Magnetic Resonance Spectroscopy at 7 T in the Rat Barrel Cortex During Whisker Activation
Published on: February 8, 2019
08:36Metabolic Mapping: Quantitative Enzyme Cytochemistry and Histochemistry to Determine the Activity of Dehydrogenases in Cells and Tissues
Published on: May 26, 2018
Related Concept Videos
01:21Huntington 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,...
01:29Hepatic Encephalopathy
DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
01:03Long-term Depression
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over time, all...
Calcium Ion Concentration Mechanism
If over time, all...
01:05Long-term Depression
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
01:22Lysosomal Hydrolases
Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
01:23Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...