Li · Psychoradiology 2026 · narrative review · n=?

Neuroimaging evidence of mitochondrial dysfunction and inflammation in psychiatric disorders: a review.

Cited 0 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Narrative review synthesizing neuroimaging modalities and mechanistic findings across psychiatric disorders.

PubMed 42436719 · doi:10.1093/psyrad/kkag023 · record verified 2026-08-28

What was done

This review examined multimodal neuroimaging techniques used to evaluate mitochondrial function (magnetic resonance spectroscopy, mitochondrial-complex PET tracers, MRI-derived cerebral metabolic rate of oxygen, T1ρ imaging, and manganese-enhanced MRI) and neuroinflammation (TSPO PET, MAO-B PET, C3aR/IL-1β-targeted tracers, and diffusion MRI) across psychiatric conditions, including schizophrenia, major depressive disorder, bipolar disorder, post-traumatic stress disorder, autism spectrum disorder, sleep disorders, and substance use disorders.

What was found

The abstract reports no numerical data, pooled effect sizes, or study counts. Qualitatively, it identified three shared transdiagnostic imaging phenotypes across disorders: impaired mitochondrial energy metabolism, altered glial cell immune activation, and white matter microstructural changes linked to neuroinflammation. It observed that very few studies have applied concurrent dual-target imaging in the same cohort to verify the direct relationship between mitochondrial dysfunction and neuroinflammation in vivo.

Why it matters

It highlights shared transdiagnostic biological targets across major psychiatric disorders and identifies technical gaps, underscoring the need for combined dual-target imaging protocols to determine how mitochondrial defects and neuroinflammation interact directly in living patients.

Limits

The review does not report quantitative metrics, search criteria, study counts, or risk-of-bias assessments in the abstract. Clinical and methodological heterogeneity across diverse psychiatric populations is substantial, and causal or direct mechanistic links between both pathways remain unverified in human cohorts.

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