# Redox therapy for neuropsychiatric disorders: Molecular mechanisms and biomarker development

## TL;DR

This review explores how redox therapy could treat brain disorders by restoring energy balance, but highlights the need for better biomarkers to track treatment effects.

## Contribution

The paper reviews molecular mechanisms of NAD-related deficits and advances in neuroimaging biomarkers for redox therapy.

## Key findings

- Redox imbalances contribute to mitochondrial dysfunction and inflammation in brain disorders.
- Current therapies show promise but lack effective in vivo biomarkers for tracking progress.
- Personalized approaches using neuroimaging biomarkers are emphasized for future treatment strategies.

## Abstract

Redox dysregulation, characterized by an imbalance in the NAD+ [nicotinamide adenine dinucleotide (oxidized form)]/NADH (reduced form of NAD+) ratio, is implicated in neurodegenerative and psychiatric disorders such as Alzheimer’s disease and schizophrenia. This imbalance contributes to mitochondrial dysregulation, oxidative stress, and inflammation. Despite promising preclinical studies supporting therapeutic strategies aimed at restoring redox balance and thereby rescuing brain bioenergetic deficits, clinical outcomes and efficacy remain limited. Progress has been hindered by the incomplete understanding of NAD+ subcellular cycling, as well as a lack of in vivo biomarkers measuring target engagement of redox status and mitochondrial function. Thus, this review examines molecular mechanisms of NAD (nicotinamide adenine dinucleotide)–related bioenergetic deficits, current and emerging NAD-targeted therapies, and recent advances in the development of neuroimaging biomarkers, emphasizing personalized and mechanism-driven approaches.

Redox therapy may restore brain energy deficits, underscoring the need for in vivo biomarkers to guide personalized treatments.