Exploration of Neuroscience

Table 2. Microbial metabolites and their mitochondrial targets in GBA.

Microbial metabolite	Primary mitochondrial target or pathway	Mechanism of action	Neurobiological/Behavioral outcome	Key references
Butyrate	HDAC inhibition; AMPK-related mitochondrial signaling	Supports mitochondrial biogenesis and redox balance in experimental systems	Reduced neuroinflammation and improved behavioral resilience in preclinical models	[17, 66, 67]
Propionate	SCFA receptor and metabolic signaling	Can influence lipid oxidation and cellular energy metabolism	Potential support for energy homeostasis and stress adaptation	[37, 68]
Acetate	Energy substrate and immune-metabolic signaling	Supports cellular respiration and may modulate neuroimmune responses	Potential reduction of neuroinflammation in preclinical settings	[37, 68]
Tryptophan metabolites (e.g., kynurenine, serotonin)	Kynurenine/NAD+ related signaling	Links microbial metabolism with redox state and serotonergic pathways	Possible effects on oxidative stress and depressive phenotypes	[18, 69]
Bile acids (secondary)	FXR/TGR5-related signaling	Can influence barrier integrity and metabolic signaling relevant to mitochondrial function	Potential support for neuronal homeostasis; evidence remains indirect	[38]
Lipopolysaccharide (LPS)	Toll-like receptor 4 (TLR4); NLRP3 inflammasome	Promotes mitochondrial stress, mtROS, and inflammatory cytokine release	Neuroinflammation and depressive-like behavior in experimental models	[73, 77, 78]

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The control of mitochondrial biogenesis and energy homeostasis involves AMPK (AMP-activated protein kinase) and PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1-alpha). Activation of SIRT1 (sirtuin 1) supports mitochondrial integrity and neuroprotection. LPS-induced TLR4 activity is associated with inflammation-related mitochondrial injury in MDD. SCFAs such as butyrate, propionate, and acetate act as metabolic and epigenetic modulators that may support neural plasticity. SCFA: short-chain fatty acid; NLRP3: nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3; MDD: major depressive disorder.

Declarations

Author contributions

OMA: Conceptualization. Data curation, Investigation, Writing—original draft, Writing—review & editing, Supervision. CAC, OEO, OCA, and ODA: Data curation, Investigation, Writing—review & editing. SJA: Writing—review & editing. All authors read and approved the submitted version.

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The authors declare that they have no conflicts of interest.

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