About

Munjal Acharya is an Associate Professor in the School of Medicine at the University of California, Irvine, with a joint appointment in Radiation Oncology. He is a member of the Chao Family Comprehensive Cancer Center and the Stem Cell Research Center. His research focuses on the neurobiological and cognitive effects of cancer treatments, including cranial radiation therapy, and the underlying mechanisms involved in cancer-related cognitive impairment. Acharya's work involves investigating neuroinflammation, neurotrophin signaling, and the role of immune checkpoints in neurocognitive functions. His contributions include exploring therapeutic strategies such as BDNF augmentation and microglial replacement to mitigate cognitive decline caused by cancer therapies and radiation exposure.

Research topics

• Medicine
• Neuroscience
• Cancer research
• Psychiatry
• Internal medicine
• Computer Science
• Biology
• Pathology
• Oncology
• Cell biology
• Immunology

Selected publications

• Supplemental Figure S6 from C5aR1 Inhibition Alleviates Cranial Radiation–Induced Cognitive Decline

  2026-01-02

  articleOpen accessSenior author

  <p>Representative images and graphical analysis of apoptotic cell marker cleaved caspase-3 in the tumor-bearing and non-mice</p>

  PublisherDOI

• Electroacupuncture improves cognitive function and neuropsychiatric symptoms in breast cancer survivors: a pilot randomized controlled trial

  JNCI Journal of the National Cancer Institute · 2026-03-31

  articleOpen access

  Abstract Background We conducted a randomized, double-blinded pilot trial to compare the impact of 2 electroacupuncture (EA) regimens on co-occurring neuropsychiatric symptoms among breast cancer survivors. Methods Breast cancer survivors (BCS) who self-reported cognitive impairment, fatigue, insomnia, or psychological distress were randomized (1:1) to receive 10 weekly EA to target either neuropsychiatric-specific (neuropsychiatric-specific EA, nEA) or nonneuropsychiatric-specific (sham EA, sEA) acupoints. Primary endpoints were the within-group pre-post effect sizes (Glass’s Δ) in symptom severities, adjusted for multiple comparisons (Padjusted). Outcomes were assessed using neurocognitive tests (CANTAB), patient-reported outcomes (PROs) (Functional Assessment of Cancer Therapy-Cognitive Function, Multidimensional Fatigue Symptom Inventory-Short Form, European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire-Core 30), plasma biomarkers, and neuroimaging. Responders were defined by reliable change index (for objective cognition) or minimal clinically important differences (for PROs). Results Thirty-five participants were recruited, with 30 (86%) completing all sessions. The mean (±SD) age was 58.2 (±12.2) years, and 86% reported co-occurring symptoms. Following treatment, the nEA group demonstrated significant improvements in attention (T3: Δ = 0.562, T4: Δ = 0.708, both Padjusted <.05) and distress (T3: Δ = 0.764, T4: Δ = 0.711, both Padjusted < .05). More responders were observed after nEA treatment for objective cognition (42.9% vs 12.5%) and distress (50% vs 37.5%). Neuropsychiatric-specific EA-treated participants showed increased gray matter volume compared with sEA (P = .033), which positively correlated with better attention function (r = 0.69, P = .020). Neuropsychiatric-specific EA-related improvements in memory and response speed were associated with reduced connectivity in the default mode network (DMN-SFG, r = −0.93, P < .01) and increased connectivity in the dorsal attention network (DAN-SMG, r = 0.86, P < .001), respectively. All adverse events were grade 2 or lower. Conclusion(s) Electroacupuncture targeting neuropsychiatric-specific acupoints suggests improvements in cognition and distress symptoms in BCS, warranting validation in larger, multicenter trials. Clinicaltrials.gov NCT05283577.

  PublisherDOI

• Supplemental Figure S1 from C5aR1 Inhibition Alleviates Cranial Radiation–Induced Cognitive Decline

  2026-01-02

  articleOpen accessSenior author

  <p>Characterization of C5aR1 expression in the WT and C5aR1 KO mice brains and blood</p>

  PublisherDOI

• Human neural stem cell-derived extracellular vesicles remediate glioblastoma therapy-induced brain fog

  Research Square · 2026-02-27

  preprintOpen accessSenior author
  PublisherOA PDFDOI

• Supplemental Table T2 from C5aR1 Inhibition Alleviates Cranial Radiation–Induced Cognitive Decline

  2026-01-02

  articleOpen accessSenior author

  <p>Affiliated gene sets for DEGs in glioblastoma tumor model</p>

  PublisherDOI

• Contributors

  Elsevier eBooks · 2026-01-01

  book-chapter
  PublisherDOI

• Supplemental Table T1 from C5aR1 Inhibition Alleviates Cranial Radiation–Induced Cognitive Decline

  2026-01-02

  articleOpen accessSenior author

  <p>Affiliated gene sets for DEGs in non-tumor model</p>

  PublisherDOI

• Human neural stem cell-derived extracellular vesicles improve cognitive function following glioma chemoradiation therapy

  Cancer Letters · 2026-05-06

  articleOpen accessSenior authorCorresponding

  ABSTRACT Cranial radiation therapy (RT) with concomitant and adjuvant temozolomide (TMZ; Stupp protocol) prolongs glioma survival but frequently results in persistent cognitive impairment. Human neural stem cell (hNSC)-derived extracellular vesicles (EVs) are a promising acellular therapy whose bioactive cargo can modulate neuroinflammation and synaptic integrity. We evaluated two EVs derived from GMP-grade hNSCs (Shef6 and UCI-191) in syngeneic glioma-bearing and non-tumor adult mice treated with fractionated cranial RT (3 × 8.67 Gy) together with concomitant low-dose (25 mg/kg) and adjuvant high-dose (66.7 mg/kg, intraperitoneal) TMZ. EV administration improved memory performance in RT-TMZ–exposed mice and, notably, Shef6-EVs also extended survival in glioma-bearing mice in the absence of chemoradiotherapy. Immunofluorescence analyses demonstrated attenuated gliosis and preservation of synaptic integrity in EV-treated RT-TMZ-exposed brains, while bulk transcriptomic profiling identified distinct neuroprotective gene expression pathways associated with each EV source. Critically, neither Shef6 nor UCI-191 EVs diminished or interfered with the anti-tumor efficacy of RT-TMZ. These data support hNSC-derived EVs as a translational strategy to mitigate treatment-related neurotoxicity while preserving oncologic benefit in a clinically relevant glioma model. • Systemic administration of GMP-grade hNSC-EVs after RT-TMZ restores cognitive performance in both non-tumor and glioma-bearing mice. • hNSC-EV treatment attenuates astrogliosis and microglial activation and preserves synaptic density in brain regions critical for learning and memory. • hNSC-EVs do not compromise the anti-tumor efficacy of RT-TMZ, as tumor control and survival are maintained in glioma-bearing animals. • Peripheral organ histology shows no gross toxicity following repeated systemic EV administration. • Transcriptomic profiling reveals distinct but convergent neuroimmune and neuroprotective gene-expression programs engaged by each EV line, consistent with the observed rescue of cognition and synaptic integrity.

  PublisherDOI

• Supplemental Figure S4 from C5aR1 Inhibition Alleviates Cranial Radiation–Induced Cognitive Decline

  2026-01-02

  articleOpen accessSenior author

  <p>Kaplan-Meier Survival Data for C5aR1-KO mice in the glioma tumor model</p>

  PublisherDOI

• Supplemental Figure S8 from C5aR1 Inhibition Alleviates Cranial Radiation–Induced Cognitive Decline

  2026-01-02

  articleOpen accessSenior author

  <p>Boxplot analysis of gene sets from Neuroinflammation Panel (NanoStringTM) across experimental groups</p>

  PublisherDOI

Frequent coauthors

• Charles L. Limoli

  University of California, Irvine

  101 shared

• Janet E. Baulch

  43 shared

• Erich Giedzinski

  40 shared

• Vipan K. Parihar

  28 shared

• Lori‐Ann Christie

  28 shared

• Leila Alikhani

  20 shared

• Katherine K. Tran

  University of California, Los Angeles

  20 shared

• Vincent J. Caiozzo

  University of California, Irvine

  19 shared