--- title: "UB Researchers Link NPAS3 Gene to Brain Energy Production — A New Target for Cognitive Disorders" slug: ub-npas3-gene-brain-energy-cognitive-disorders-2026 category: health category_label: "Health" author: "BrainWavePost Staff" date: 2026-06-18 tags: ["mental health", "neuroscience", "NPAS3", "astrocytes", "mitochondria", "schizophrenia", "University at Buffalo"] read_time_minutes: 6 canonical_url: https://brainwavepost.com/article/ub-npas3-gene-brain-energy-cognitive-disorders-2026 source: BrainWavePost --- # UB Researchers Link NPAS3 Gene to Brain Energy Production — A New Target for Cognitive Disorders *Health · 2026-06-18 · BrainWavePost Staff · 6 min read* > University at Buffalo scientists have shown that the NPAS3 gene controls how astrocytes power the brain — a discovery published in Science Advances that points to a new target for schizophrenia, bipolar disorder and autism. > **How this article is sourced** _(info)_ > > All claims are drawn from primary sources: the University at Buffalo news release of 18 June 2026, the peer-reviewed study published in Science Advances (AAAS), and supporting reporting from Medical Xpress, News-Medical.Net and the Jacobs School of Medicine and Biomedical Sciences. [1][2][3][4][5] Researchers at the Jacobs School of Medicine and Biomedical Sciences at the University at Buffalo (UB) have identified a specific gene — NPAS3 — that controls how brain support cells generate the energy required for thinking, learning and memory. [1][2] The findings, published on 18 June 2026 in the AAAS journal Science Advances, point to a new molecular target for cognitive symptoms in disorders such as schizophrenia, bipolar disorder and autism. [1][2] ## What the researchers found Led by Mikhail V. Pletnikov, MD, PhD, professor and chair of UB's Department of Physiology and Biophysics, and first author Kateryna Murlanova, PhD, the team showed that NPAS3 — a transcription factor that regulates how other genes are switched on — controls mitochondrial energy production specifically in astrocytes, the star-shaped support cells that make up roughly half of all brain cells. [1][2][3] - When NPAS3 was selectively removed from astrocytes in mice, the astrocytes produced less energy in their mitochondria. [1][2] - Those mice then performed poorly on standard learning and memory tests. [1][2][3] - Giving the mice lactate — a by-product of cellular energy metabolism the brain can use as fuel — largely corrected the deficit and restored learning and memory performance. [1][2] > Previous studies have linked NPAS3 to conditions involving cognitive problems, such as schizophrenia, but scientists didn't know exactly how it might be involved. This study demonstrates a mechanistic link between NPAS3-dependent astrocyte mitochondria bioenergetics and cognitive function. > > — Mikhail Pletnikov and Kateryna Murlanova, University at Buffalo news release, 18 June 2026 [1] ## Why astrocytes matter Astrocytes were long viewed as passive 'glue' that simply held neurons in place. Over the past decade, neuroscience has reframed them as active partners in brain metabolism, ion balance and synaptic signalling. [1][3] The UB study reinforces that view by showing that an astrocyte-specific energy defect — driven by loss of a single transcription factor — is enough to produce measurable cognitive impairment in mice. [1][2] Because astrocytes make up about half of all brain cells, drugs that target their metabolism could in principle reach a much larger fraction of brain tissue than therapies aimed only at neurons. [1] That is one reason the authors describe astrocyte bioenergetics as a 'new target' for psychiatric and neurological disorders that have historically been hard to treat. [1][3] - **NPAS3** — Transcription factor regulating astrocyte mitochondrial energy production [1][2] - **~50%** — Share of brain cells that are astrocytes [1] - **Science Advances** — AAAS journal where the peer-reviewed study was published, 18 Jun 2026 [2] ## From a Hopkins family pedigree to a UB lab Pletnikov began studying NPAS3 more than a decade ago at Johns Hopkins, after collaborators identified a mutation in a family whose members had severe neurological and psychiatric disorders and suspected NPAS3 insufficiency as a factor. [1] That clinical observation pushed his research toward glial cells — non-neuronal support cells — and their metabolism, work he has continued at UB with Murlanova, who trained in his Hopkins lab before joining him in Buffalo. [1][3] The current paper is the result of a multi-institutional collaboration that includes researchers at Roswell Park Comprehensive Cancer Center, the Danish Research Institute of Translational Neuroscience, Kyungpook National University and the Korea Brain Research Institute, Johns Hopkins, Case Western Reserve, the Brain Health Medicines Center in Cleveland, and the Louis Stokes VA Medical Center. [1] ## What it could mean for treatment Cognitive symptoms in conditions like schizophrenia — memory problems, attention deficits and impaired executive function — are among the hardest to treat with existing medications, which mostly target neurotransmitter systems rather than cellular metabolism. [1][3] By pointing to NPAS3-driven astrocyte bioenergetics as a distinct mechanism, the UB work suggests that future drugs could aim to support or restore mitochondrial energy production in glial cells. [1][2] The authors are cautious about over-reading the lactate experiment: Pletnikov stresses that lactate is not about to become a treatment for schizophrenia, and that the immediate value of the finding is mechanistic — it tells researchers where to look next. [1] He and Murlanova are now preparing a grant application focused on mental-health treatments that build on these metabolic pathways. [1] > **Why this matters for mental-health research** _(tip)_ > > Decades of psychiatric drug development have focused almost exclusively on neurons and neurotransmitters. Findings like this one — placing astrocyte metabolism at the centre of cognition — broaden the search for treatments and align with the wider 2026 push to give serious mental-health research the visibility and funding it has historically lacked. [1][3][4] ## Limitations to keep in mind The study was conducted in mice with NPAS3 selectively deleted from astrocytes — a powerful model for dissecting mechanism, but not a direct test in human patients. [1][2] Translating these findings into therapies will require showing that the same NPAS3–astrocyte–mitochondria axis operates in human brain tissue, identifying drug-like molecules that can safely modulate it, and demonstrating cognitive benefit in clinical trials. [1][2][3] None of that has yet been done. ## The bottom line A single transcription factor in a single class of brain support cells appears to gate the energy supply that thinking depends on. That is a clean, testable mechanism — and a credible new entry point for treating cognitive symptoms in some of the most disabling psychiatric and neurological disorders. [1][2][3] ## Sources (clickable) - [1] University at Buffalo News — 'Gene tied to energy production in brain could lead to new treatment for cognitive disorders' (18 Jun 2026): https://www.buffalo.edu/news/releases/2026/06/NPAS3-study-brain-health.html - [2] Science Advances (AAAS) — Murlanova et al., peer-reviewed study on NPAS3, astrocyte bioenergetics and cognition (18 Jun 2026): https://www.science.org/doi/10.1126/sciadv.adt2527 - [3] Jacobs School of Medicine and Biomedical Sciences, University at Buffalo — Department of Physiology and Biophysics (Pletnikov lab): https://medicine.buffalo.edu/departments/physiology.html - [4] Mikhail V. Pletnikov, MD, PhD — faculty profile, Jacobs School of Medicine: https://medicine.buffalo.edu/faculty/profile.html?ubit=mvpletni - [5] Kateryna Murlanova, PhD — ORCID research profile: https://orcid.org/0000-0001-9236-6648 --- _Canonical article: [https://brainwavepost.com/article/ub-npas3-gene-brain-energy-cognitive-disorders-2026](https://brainwavepost.com/article/ub-npas3-gene-brain-energy-cognitive-disorders-2026) — © BrainWavePost. Educational content; see the article page for full disclaimers._