# Glial lactate metabolism and transport in Alzheimer’s disease

## TL;DR

This paper reviews how changes in glial lactate metabolism contribute to Alzheimer's disease progression and potential new treatment strategies.

## Contribution

The paper provides a synthesis of recent findings on stage-specific glial lactate metabolism and its role in Alzheimer's.

## Key findings

- Disrupted glial lactate metabolism contributes to neuronal energy crisis in Alzheimer’s disease.
- Altered lactate shuttle systems via MCTs and gap junctions are linked to neuroinflammation in AD.
- Understanding glial lactate dynamics may lead to new AD biomarkers and therapies.

## Abstract

Emerging evidence suggests that lactate, once considered merely a metabolic byproduct, plays vital roles in brain energy metabolism, signaling, and neuroprotection. In Alzheimer’s disease (AD), increasing research has implicated disruptions in glial lactate metabolism and transport as key contributors to neurodegenerative progression. This review synthesizes recent findings on the dynamic metabolic profiles of astrocytes, oligodendrocytes, and microglia, with emphasis on their stage-specific glycolytic activities and their roles in neuronal energy support. We detail how these cellular metabolic behaviors and the intercellular lactate shuttle systems—mediated by monocarboxylate transporters (MCTs) and gap junctions—are altered in AD pathology. We highlight how these changes lead to a state of neuronal energetic crisis and, paradoxically, contribute to neuroinflammation. A clearer understanding of these complex glial lactate dynamics offers a promising perspective for novel AD biomarkers and therapeutic strategies.