Is a deficiency of dopamine the only reason for Parkinsons? Actually, there are many causes of Parkinsons which include toxins, trauma and infections.

Some people take medications or supplements to boost dopamine levels. They welcome a temporary relief of symptoms. A conclusion drawn particularly by individuals who celebrate quick, though temporary relief, is that the only cause of symptoms centers on dopamine deficiencies.
Actually, infections are only one of the many causes of Parkinsons. Not convinced? Consider research that links Tuberculosis to Parkinsons, an infection becoming more prevalent in many countries.
I know. You are probably thinking: How could there be any connection between Tuberculosis and Parkinsons?
The study abstracts below document that there is a connection between Tuberculosis and Parkinsons. And get this. Tuberculosis is only one among other infections that have been documented to cause neurological problems. Others include Lyme disease, Mononucleosis, Epstein Barr and many others as well.
The study abstracts below document that there is a connection between Tuberculosis and Parkinsons. And get this. Tuberculosis is only one among other infections documented by studies to cause neurological problems. Others include Lyme disease, Mononucleosis, Epstein Barr and others as well.

For some people, dopamine deficiencies play a minor role when it comes to identifying the cause of symptoms. Recovery for some people requires treating infections that may be contributing to their symptoms. Taking L-dopa supplements or medications do not address infections in the body, though they may offer temporary relief.
Tuberculosis is one of Many Causes of Parkinsons
Can J Neurol Sci. 2025 Sep 29:1-10. Movement Disorders in Central Nervous System Tuberculosis: A Systematic Review
Abstract
Background: Tuberculosis (TB) affecting the central nervous system (CNS) can lead to a broad range of movement disorders, which are frequently overlooked in clinical settings. This review explores the various presentations, underlying mechanisms and patient outcomes related to these disorders.
Methods: We systematically reviewed published case reports, series and cohort studies that described patients with CNS TB who developed movement disorders. Extracted data included patient characteristics, type of CNS TB, imaging and CSF findings, types of movement disorders, treatments used and outcomes.
Results: A total of 61 patients with CNS TB and associated movement disorders were analyzed. The most common manifestations were ataxia, dystonia, chorea or hemiballismus and parkinsonism. Less frequent symptoms included opsoclonus-myoclonus, segmental myoclonus, tremors, cervical dystonia and stereotypy. TB meningitis was the predominant form, often accompanied by infarcts, hydrocephalus or tuberculomas. Proposed causes included vascular injury, inflammatory lesions, immune mechanisms and drug-related effects. All patients received anti-tuberculosis treatment, and nearly half required corticosteroids or surgical procedures. About 25 patients (41%) fully recovered, 17 (27.9%) had significant improvement, 13 (21.3%) showed partial improvement, 11 (18.0%) had ongoing problems and 1 (1.6%) died. Cohort studies also reveal that movement disorders – particularly tremors, dystonia, parkinsonism and ataxia – are frequent but underrecognized in CNS TB. These typically emerge early, often within three weeks, and are linked to lesions in the basal ganglia or thalamus.
Conclusions: Movement disorders in CNS TB are more common than generally recognized. Prompt diagnosis through imaging and timely therapy can greatly improve neurological outcomes.
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Tuberculosis (Edinb). 2025 Jul:153:102653. Hippocampal syndrome secondary to tuberculosis: From neuroinflammation to neurodegeneration
Abstract
Background: Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a primary global health concern, with significant long-term sequelae. Central nervous system TB (CNS-TB) is a clinical spectrum with entities such as tuberculous meningitis and tuberculomas. Emerging evidence suggests that Mtb may directly or indirectly affect the hippocampus, a critical memory, learning, and cognition structure.
Objectives: This review aims to summarize the current biological understanding of Mtb’s impact on the hippocampus, elucidate its potential role in neurodegeneration, and introduce the concept of “Hippocampal syndrome secondary to tuberculosis (HSST)” as a novel chronic entity within the CNS-TB spectrum.
Methods: A comprehensive literature review was conducted to analyze how Mtb gains access to the brain, its neurotropism, and the resulting neuroinflammatory and neurodegenerative effects on the hippocampus. Data from clinical, histopathological, and experimental studies were evaluated to assess potential links between TB and cognitive impairment.
Results: Mtb can access the CNS through hematogenous dissemination, the “Trojan Horse” mechanism, or via the olfactory pathway, bypassing the blood-brain barrier (BBB). Once in the brain, Mtb induces chronic neuroinflammation and disrupts hippocampal structure. Studies suggest that TB increases the risk of Alzheimer’s and Parkinson’s diseases, with evidence of Mtb-driven amyloid-beta accumulation and neuronal loss. Furthermore, specific Mtb strains exhibit neurotropism and produce virulence factors that facilitate CNS invasion.
Conclusions: Understanding the interaction between TB and neurocognitive disorders is critical for improving post-TB care. Recognizing HSST as a chronic condition within the CNS-TB spectrum may support early diagnosis and targeted interventions to mitigate long-term neurological consequences.
Microorganisms. 2024 Sep 13;12(9):1890. Mycobacterium paratuberculosis: A HERV Turn-On for Autoimmunity, Neurodegeneration, and Cancer?
Mycobacterium paratuberculosis: A HERV Turn-On for Autoimmunity, Neurodegeneration, and Cancer?
Abstract
Human endogenous retroviruses (HERVs) are remnants of ancient retroviral infections that, over millions of years, became integrated into the human genome. While normally inactive, environmental stimuli such as infections have contributed to the transcriptional reactivation of HERV-promoting pathological conditions, including the development of autoimmunity, neurodegenerative disease and cancer.
What infections trigger HERV activation? Mycobacterium avium subspecies paratuberculosis (MAP) is a pluripotent driver of human disease. Aside from granulomatous diseases, Crohn’s disease, sarcoidosis and Blau syndrome, MAP is associated with autoimmune disease: type one diabetes (T1D), multiple sclerosis (MS), rheumatoid arthritis (RA) and autoimmune thyroiditis. MAP is also associated with Alzheimer’s disease (AD) and Parkinson’s disease (PD). Autoimmune diabetes, MS and RA are the diseases with the strongest MAP/HERV association.
Med Hypotheses. 2002 Oct;59(4):373-7. Parkinson’s: another look
Abstract
Recent studies in the Parkinson’s literature have cited a tuberculosis-like germ called Nocardia as being responsible for Parkinson’s disease. Kohbata seemingly cemented a relationship between Nocardia and Parkinson’s by finding serologic evidence in 20 of 20 Parkinson’s patients, acknowledging that blood tests for Nocardia and the mycobacteria such as tuberculosis often cross-react, as they belong to the same order of bacteria, the Actinomycetales. Besides this difficulty in differentiation, a well-used medical school textbook of microbiology, Atlas, points out that even among experts, different observers may classify the same strain of bacteria as Nocardia or Mycobacterium tuberculosis.
Parkinson’s: another look is a theoretical article which presents compelling, well-documented evidence for an infectious cause for Parkinson’s disease on historical, epidemiological, pharmacologic, microbiological, and biochemical levels.




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