Evidence map›Paper›PMID 42862481›Full record

ReviewNeurochemical research2026

PPARγ Signaling in the Central Nervous System: A Review of the Implications in Synaptic Plasticity, Neuroinflammatory and Neoplastic Processes.

Vanessa Camylla Bernardo de Oliveira Maciel, Josenilda de Moura Arruda, Ryan Cordeiro Silva, Michelle Melgarejo da Rosa

Abstract readReview
In one paragraph

Review in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Vanessa Camylla Bernardo de Oliveira MacielLaboratory of Immunomodulation and New Therapeutic Approaches (LINAT), Nucleus of Research in Therapeutic Innovation Suely Galdino (NUPIT-SG), Biosciences Center, Federal University of Pernambuco, Recife, Brazil.ORCID http://orcid.org/0000-0001-5398-1277
Josenilda de Moura ArrudaLaboratory of Immunomodulation and New Therapeutic Approaches (LINAT), Nucleus of Research in Therapeutic Innovation Suely Galdino (NUPIT-SG), Biosciences Center, Federal University of Pernambuco, Recife, Brazil.ORCID http://orcid.org/0009-0003-7087-5742
Ryan Cordeiro SilvaLaboratory of Immunomodulation and New Therapeutic Approaches (LINAT), Nucleus of Research in Therapeutic Innovation Suely Galdino (NUPIT-SG), Biosciences Center, Federal University of Pernambuco, Recife, Brazil.ORCID http://orcid.org/0000-0002-2988-6787
Michelle Melgarejo da RosaLaboratory of Immunomodulation and New Therapeutic Approaches (LINAT), Nucleus of Research in Therapeutic Innovation Suely Galdino (NUPIT-SG), Biosciences Center, Federal University of Pernambuco, Recife, Brazil. michelle.rosa@ufpe.br.ORCID http://orcid.org/0000-0002-0163-3833

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peroxisome proliferator activated receptor gamma (PPARγ) is a ligand activated nuclear receptor traditionally associated with lipid and glucose metabolism. Emerging evidence, however, identifies PPARγ as a central immunometabolic regulator in the central nervous system (CNS), coordinating mitochondrial function, neuroinflammation, synaptic plasticity, and neurovascular integrity. Beyond its classical metabolic actions, PPARγ regulates microglial activation, astrocytic inflammatory responses, oxidative stress, and mitochondrial biogenesis, thereby influencing neuronal resilience and circuit stability. This narrative review synthesizes knowledge of PPARγ structure, activation, CNS distribution, endogenous ligands, and synthetic agonists, including thiazolidinediones and selective modulators. We highlight how PPARγ controls transcriptional programs related to energy homeostasis, inflammatory signaling, including NF κB dependent pathways, and blood brain barrier function. Attention is devoted to synaptic remodeling and plasticity, positioning PPARγ as a molecular bridge between metabolic state and neuronal adaptability. We propose that PPARγ signaling dysregulation represents a convergent mechanism in neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and adrenoleukodystrophy; psychiatric conditions, such as depression and anxiety; and neurooncological processes. Integrating evidence across these conditions supports PPARγ as a master regulator of neuroimmune metabolic coupling in the brain. Finally, we discuss translational challenges and opportunities, including brain penetrant, functionally selective ligands, clarification of cell type specific signaling, and expansion of rigorous clinical trials. Integrating mechanistic, preclinical, and clinical trial evidence, this review critically examines the therapeutic potential of PPARγ across neurodegenerative, psychiatric, and neurooncological CNS conditions, while identifying priorities for future therapeutic development in diverse brain disorders.

Indexed as

Central Nervous SystemNeuroinflammatory DiseasesNeuronal PlasticityPPAR gammaSignal TransductionAnimalsHumansPPAR-gamma AgonistsPPAR gammaPPAR-gamma AgonistsNeuroinflammationPPARγSynaptic plasticitySynaptic remodelingThiazolidinediones

Identifiers

PMID42862481
PMCPMC13658551

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.