Research Repository
Research into neuroinflammatory brain disorders is rapidly evolving, revealing how immune system activation — particularly in response to infections — can contribute to the onset, progression, and variability of a wide range of neurological and secondary psychiatric conditions.
Patients with immune-mediated disorders are at increased risk for neuropsychiatric symptoms. This section provides access to current studies, emerging findings, and disorder-specific research that explores the immune mechanisms driving neuroinflammation that contributes to these disorders as well as related psychiatric conditions. Each disorder featured includes links to publications, key themes in pathophysiology, and areas of ongoing investigation.
Access Research Based by Condition
Alzheimer's Disease
Alzheimer’s Disease research suggests its causes may be broader than once thought. The disease may reflect an infection-inflammation model, where immune dysregulation, pathogen exposure, and neuroinflammation drive cognitive decline, often accompanied by neuropsychiatric symptoms.
Autism
Autism Spectrum Disorder is a complex neurodevelopmental condition with multiple contributing factors. In some cases—particularly during critical periods of development—infection-triggered immune activation and neuroinflammation may influence symptom emergence in some children.
Bartonellosis
Bartonellosis can provoke persistent neurological and psychiatric symptoms through immune-mediated mechanisms. Neuroinflammation, cytokine dysregulation, and autoimmunity may explain cognitive deficits, seizures, and encephalopathy after infection.
Candida
Candida infections may affect CNS function in some individuals through neuroinflammation, gut-brain axis disruption, and immune-mediated mechanisms, emphasizing early recognition to reduce long-term cognitive and psychiatric effects.
Crohn's
Crohn’s disease reflects complex interactions between pathogens, immunity, and neuroinflammation. Dysregulated gut-brain signaling may underlie both intestinal flares and systemic neuropsychiatric manifestations.
Encephalitis
Encephalitis can arise from CNS infection or immune-mediated responses to pathogens. Infectious and autoimmune encephalitis can lead to blood-brain barrier disruption, allowing immune cells and cytokines to infiltrate the CNS. The resulting neuroinflammation often manifests as psychiatric symptoms.
Hashimoto's Thyroiditis
Hashimoto’s Thyroiditis is an autoimmune thyroid disorder that involves a complex interplay of genetic susceptibility and environmental triggers, including infection. The potential neuropsychiatric effects may precede overt thyroid dysfunction.
Heart Disease
Heart disease is increasingly linked to infections—from viruses to bacteria—that trigger immune responses, vascular inflammation, and autoimmunity. These processes can also impact the brain, contributing to neuroinflammation and cognitive or mood disturbances.
Infection-Associated Delirium in Older Adults
Long COVID
Long COVID is a post-viral syndrome where persistent immune dysregulation and neuroinflammation drive fatigue, cognitive dysfunction, and neuropsychiatric symptoms, highlighting lasting effects of infection on brain and systemic health.
Lyme
Lyme disease results from an infection, transmitted through the tick bite, with immune and neuroinflammatory responses. This can drive neurological and psychiatric manifestations. Persistent antigens in the central nervous system can lead to sustained inflammation, even after antimicrobial therapy.
Narcolepsy
Narcolepsy is a neurological disorder linked to influenza A and group A Streptococcus infections. In susceptible patients, immune cross-reactivity triggers neuroinflammation and hypocretin neuron loss, contributing to neuropsychiatric symptoms such as depression, anxiety, and cognitive deficits.
NMaDAR Encephalitis
NMaDAR Encephalitis is an autoimmune neuropsychiatric disorder where post-infectious immune dysregulation triggers antibodies against NMDARs, producing acute psychiatric symptoms, seizures, and movement disorders via neuroinflammation.
OCD (Obsessive-compulsive disorder)
OCD is a complex neuropsychiatric disorder with well-established neurobiological underpinnings. In certain cases—particularly in children—the acute emergence of symptoms following infection suggests an immune-mediated pathophysiology.
PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections)
PANDAS represents a clinically distinct post-streptococcal neuropsychiatric syndrome involving abrupt-onset OCD and/or tics following infection. Proposed mechanisms include neuroinflammation and pathogenic autoantibodies affecting basal ganglia function.
PANS (Pediatric Acute-Onset Neuropsychiatric Syndrome)
PANS is characterized by the abrupt onset of OCD and/or severe eating restriction, along with additional symptoms such as anxiety, mood lability, or neurologic changes. This immune-mediated, neuroinflammatory condition may be triggered by various physiological stressors, including infections.
Parkinson's Disease
Parkinson’s Disease may be influenced by infections that trigger neuroinflammation and alpha-synuclein pathology. Viral and bacterial agents, gut dysbiosis, and immune activation are increasingly recognized as contributors to both motor and neuropsychiatric features.
Postpartum
Postpartum neuropsychiatric risk is heightened by infection-triggered immune responses. Infections during pregnancy or postpartum, may trigger immune-mediated neuroinflammation, disrupting neurotransmitter systems and contributing to depression, anxiety, or OCD.
POTS and Dysautonomia
POTS and Dysautonomia can follow viral or bacterial infections, such as Epstein-Barr virus, influenza, or COVID-19. Immune activation, autoantibodies, and neuroinflammation may impair autonomic regulation, resulting in diverse cardiovascular and neuropsychiatric manifestations.
Restrictive Food Intake Disorder
Restricted Food Intake Disorder may arise from infection-related neuroinflammation, where immune responses disrupt neural circuits controlling appetite, fear, and sensory processing resulting in food avoidance. Key mechanisms include molecular mimicry and Blood Brain Barrier disruption.
Rocky Mountain Spotted Fever (Rickettsia rickettsii)
Rocky Mountain Spotted Fever is an acute tick-borne infection that can trigger systemic and CNS inflammation. Endothelial injury, cytokine cascades, and neuroinflammation may lead to encephalopathy, cognitive changes, and rare neuropsychiatric sequelae.
Sydenham's Chorea
Sydenham chorea is a post-streptococcal autoimmune disorder linking infection, basal ganglia inflammation, and dopamine dysregulation. Neuropsychiatric symptoms are frequently observed and can precede, coincide with, or follow motor symptoms. Understanding SC informs broader neuroimmune research.
Syphilis
Syphilis exemplifies how persistent infection can drive chronic neuroinflammation with diverse neuropsychiatric outcomes. Clinical manifestations vary from mild cognitive impairment and mood disturbances to severe dementia, psychosis, and personality changes.
Toxoplasmosis
Toxoplasmosis establishes latent CNS infection, inducing microglial activation and immune-mediated neuroinflammation. These effects can modulate behavior, cognition, and, in some cases, psychiatric symptom emergence.
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