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Abnormal substrate levels that depend upon mitochondrial function in cerebrospinal fluid from Alzheimer patients
N Redjems-Bennani1, C Jeandel, E Lefebvre
1Laboratoire de Pathologie Cellulaire et Moléculaire en Nutrition, EP616 CNRS, Faculté de Médecine, Université de Nancy I, France.
Gerontology
|August 7, 1998
Summary
Alzheimer's disease impairs brain cell metabolism. Key molecules in the tricarboxylic acid cycle, like succinate and fumarate, were significantly altered in Alzheimer's patients' cerebrospinal fluid.
Area of Science:
- Neuroscience
- Biochemistry
- Metabolomics
Background:
- Impaired oxidative and energy metabolism are hallmarks of Alzheimer's disease (AD).
- These metabolic disruptions correlate with cognitive decline and functional deficits in AD patients.
Purpose of the Study:
- To investigate alterations in mitochondrial function in Alzheimer's disease.
- Quantitatively analyze substrates of the tricarboxylic acid cycle in cerebrospinal fluid (CSF) of AD patients.
Main Methods:
- Utilized gas chromatography/mass spectrometry to measure organic acids in CSF from 17 AD patients and 17 controls.
- Determined CSF glucose and glutamine concentrations via enzymatic and ion exchange chromatography methods.
Main Results:
- Alzheimer's patients exhibited significantly higher CSF lactate levels (p = 0.002).
- Patients showed significantly lower mean CSF levels of succinate (p = 0.002), fumarate (p = 0.003), and glutamine (p = 0.0005).
- CSF glucose levels remained unchanged between groups.
Conclusions:
- Findings suggest a significant impairment of mitochondrial oxidative metabolism in the brain cells of individuals with Alzheimer's disease.
- Metabolic alterations identified may contribute to the pathogenesis and progression of Alzheimer's disease.