# Normal cerebral oxygen consumption and lactate levels in patients with Alzheimer’s disease and Lewy body dementia

## TL;DR

This study found no evidence of tissue hypoxia in Alzheimer’s and Lewy body dementia patients, suggesting brain metabolism issues are due to neurodegeneration, not low oxygen.

## Contribution

The study challenges the hypothesis that hypometabolism in dementia is caused by tissue hypoxia, offering new insights into its underlying mechanisms.

## Key findings

- No significant differences in brain lactate or oxygen metabolism were found between dementia patients and controls.
- Reduced blood flow in the precuneus of Alzheimer’s patients was not linked to higher lactate levels.
- Hypometabolism in dementia likely reflects neurodegeneration rather than hypoxia.

## Abstract

Brain metabolism is reduced in patients with dementia disorders, as demonstrated by hypometabolism on 2-deoxy-2-[18F]fluoroglucose ([18F]FDG) positron emissions tomography. A contributing factor to the hypometabolism could be decreased cerebral blood flow (CBF) leading to a state of subtle hypoperfusion‐induced tissue hypoxia causing a reduced brain oxygen metabolism and consequently elevated brain lactate. In the current exploratory study, we investigated brain lactate, global and regional CBF, and global cerebral metabolic rate of oxygen (CMRO2) in patients with Alzheimer’s disease (AD) and dementia with Lewy bodies (DLBs). We hypothesized that the patients demonstrate a state of tissue hypoxia with reduced CMRO2 and elevated brain lactate concentration. Participants included 24 AD patients, 10 DLB patients, and 15 healthy controls. MR spectroscopy measured lactate in the precuneus and occipital lobe. Global CBF and venous oxygen saturation (for CMRO2 calculation) were assessed using phase-contrast and susceptibility-based oximetry MRI, respectively. Regional CBF was measured with ASL-MRI. We observed no significant difference in either brain lactate or CMRO2 between groups. The regional CBF in precuneus was significantly lower in AD compared to HC; however, this hypoperfusion was not associated with a higher lactate concentration. The lack of a difference in CMRO2 or lactate concentration between patients and controls suggests that the hypometabolism observed in patients with AD and DLB may reflect structural neurodegeneration and not a state of tissue hypoxia. The local decrease of CBF in precuneus in patients with AD may be due to a lower CBF demand due to neurodegeneration.