Posts by:
Gabriella True

Bartonella henselae, Babesia odocoilei and Babesia divergens-like MO-1 infection in the brain of a child with seizures, mycotoxin exposure and suspected Rasmussen’s encephalitis
Breitschwerdt EB, Maggi RG, Robveille C, Kingston E. Bartonella henselae, Babesia odocoilei and Babesia divergens-like MO-1 infection in the brain of a child with seizures, mycotoxin exposure and suspected Rasmussen’s encephalitis. J Cent Nerv Syst Dis. 2025 Mar 12;17:11795735251322456. doi: 10.1177/11795735251322456. PMID: 40083671; PMCID: PMC11905044.
  • Despite cat and suspected tick exposure, Bartonella henselae and Borrelia burgdorferi serology remained negative.
  • Neurodiagnostic testing partially supported Rasmussen’s encephalitis; brain biopsy showed astrogliosis.
  • Bartonella henselae DNA was detected in brain tissue cultures.
  • Babesia odocoilei and Babesia divergens-like MO-1 were confirmed in blood and brain tissue from 2022–2023.
  • Infections, compounded by mycotoxin exposure, created a complex clinical case.
Obsessive Compulsive Disorder associated with Autoimmunity in Youth: Clinical Course before and after Rituximab+/- Adjunctive Immunomodulation
Frankovich J, Calaprice D, Ma M, Knight O, Miles K, Manko C, Hernandez JD, Sandberg J, Farhadian B, Xie Y, Silverman M, Madan J, Strand V, Chang K, Thienemann M. Obsessive Compulsive Disorder associated with Autoimmunity in Youth: Clinical Course before and after Rituximab+/- Adjunctive Immunomodulation. Dev Neurosci. 2025 Mar 10:1-26. doi: 10.1159/000544993. Epub ahead of print. PMID: 40064151.
  • Case review (n=23) from Stanford on their use of rituximab for presumed-neuroimmune and severe OCD in youth
  • Some (47.8%) experienced transient increases in psychiatric or joint pain symptoms before signs of improvement. The time frame for signs of improvement was 3-4 months. 
  • 70% achieved full or partial recovery at 1-5 years.
  • Receiving adjunct immunomodulation was associated with a higher likelihood of achieving full or partial recovery compared with those without adjunct immunomodulation
Microglia dysfunction, neurovascular inflammation and focal neuropathologies are linked to IL-1- and IL-6-related systemic inflammation in COVID-19

Fekete, R., Simats, A., Bíró, E., Pósfai, B., Cserép, C., Schwarcz, A., Szabadits, E., Környei, Z., Tóth, K., Fichó, E., Szalma, J., Vida, S., Kellermayer, A., Dávid, C., Acsády, L., Kontra, L., Silvestre-Roig, C., Moldvay, J., … Dénes, Á. (2025). Microglia dysfunction, neurovascular inflammation and focal neuropathologies are linked to IL-1- and IL-6-related systemic inflammation in COVID-19. Nature Neuroscience, 28(3), 558–576. DOI: 10.1038/s41593-025-01871-z

  • Neuropathological study examining brains of individuals with COVID-19.

  • Identifies microglial dysfunction, astrocyte involvement, and neurovascular inflammation linked to systemic IL-1 and IL-6 signaling.

  • Demonstrates blood–brain barrier disruption and gliovascular pathology even in the absence of direct viral invasion of brain tissue.

  • Provides strong evidence for self-sustaining inflammatory loops between peripheral immune signals and CNS cells.

Microglia dysfunction, neurovascular inflammation and focal neuropathologies are linked to IL-1- and IL-6-related systemic inflammation in COVID-19

Fekete R, Simats A, Bíró E, et al. Microglia dysfunction, neurovascular inflammation and focal neuropathologies are linked to IL-1- and IL-6-related systemic inflammation in COVID-19. Nat Neurosci. 2025;28(3):558-576. doi:10.1038/s41593-025-01871-z.

Impaired microglia function and vascular inflammation in COVID

  • Observational study evaluating Long COVID patients treated with H1/H2 antihistamines.

  • Reports improvement in fatigue, cognitive symptoms, tachycardia, and other systemic complaints.

  • Supports the hypothesis that mast cell activation contributes to Long COVID symptom persistence.

  • Suggests immune dysregulation—rather than viral persistence—may drive ongoing symptoms in a subset of patients.

IVIG Stopped Ella’s Self-Harm
IVIG Stopped Ella’s Self-Harm

Trigger Warning: Self-Harm & Suicide The following story discusses experiences with self-harm, suicidal thoughts, and psychiatric hospitalization. If you are sensitive to these topics, please...

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Neuroinflammation and pathways that contribute to Tourette Syndrome

Wu, X., Hao, J., Jiang, K. et al. Neuroinflammation and pathways that contribute to tourette syndrome. Ital J Pediatr 51, 63 (2025). https://doi.org/10.1186/s13052-025-01874-3

Read a deeper dive: Neuroinflammation and Immune Pathways in Tourette Syndrome

  • Tourette Syndrome (TS): A neurodevelopmental disorder characterized by motor and vocal tics, often co-occurring with ADHD, OCD, and other psychological issues.
  • Neurotransmitter Imbalances: TS is traditionally linked to neurotransmitter disruptions, especially within the cortex-striatum-thalamus-cortex circuit, involving dopamine and glutamate.
  • Neuroinflammation: Emerging research shows neuroinflammation, often triggered by infections or allergies, contributes to neurotransmitter imbalances that may induce tics.
  • Infectious Triggers: Streptococcal infections (e.g., PANDAS), viral infections (e.g., enterovirus, COVID-19), and other pathogens (e.g., Chlamydia, Mycoplasma) are linked to TS exacerbation.
  • Immune Mechanisms: Inflammatory responses activate microglia and the peripheral immune system, disrupting neurotransmitter balance and leading to tics.