Hypothesis
Jennifer M. Thornton and Jenny L. Stevenson
Emerging evidence suggests that various microbes and mites may play a significant role in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease (AD), Lewy body dementia (LBD), and Parkinson's disease (PD). The association between microbial exposure and these conditions raises the possibility that mites, as vectors or direct agents, could contribute to disease onset and progression. PD, with 15% or less of cases linked to genetics, highlights the importance of environmental factors in the remaining sporadic cases. Mites, known to harbor prions, suggest a potential mechanism for horizontal transmission. Mites can inject neurotoxins that may disrupt neurological systems, potentially leading to movement disorders, memory loss, and cognitive decline. Conditions like seborrheic dermatitis and rosacea, linked to mites such as Demodex, are highly prevalent in patients with PD and AD, and mite-induced inflammation may exacerbate disease symptoms. Mite infestations can cause systemic illness, including respiratory, gastrointestinal, and neurological disturbances. Due to their microscopic size, they are often undetected and potentially can swap DNA with humans. This article summarizes observations linking mite exposure to neurodegenerative diseases. In one family, a member was diagnosed with LBD following chronic skin issues and mite exposure, while another developed symptoms associated with PD. Mites may contribute through prion transmission, neurotoxin injection, or by triggering inflammation. A nationwide study found that scabies patients treated with lindane, a neurotoxic pesticide, had a significantly reduced PD risk, suggesting a protective effect. These findings underscore the urgent need for further research into mites and environmental triggers. Click to Read the Article
Lewy bodies are a hallmark of Parkinson's Disease. Lewy body dementia is characterized by Lewy bodies in the brain and often co-occurs with Alzheimer’s Disease (AD) pathology, including amyloid plaques and tau tangles. Around 50% of people with AD have Lewy body pathology (Marsh et al)
Saving My Family: The Rise of Parkinson's and Other Diseases documents real world disease progression before diagnoses were confirmed. Available on Amazon
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It is plausible that arthropods, such as Demodex mites commonly present on human skin, interact with coronaviruses through molecular attraction—specifically between the chitin in their exoskeletons and the lipids in the SARS-CoV-2 viral envelope (Tatu et. al). This suggests Demodex might play an under-recognized role as cofactors in viral transmission, a possibility that could carry significant implications for both disease prevention and treatment strategies.
In a recent study, researchers found that administering the SARS-CoV-2 spike protein intravenously triggered neuroinflammation and led to the buildup of alpha-synuclein in brain areas associated with PD (Schreiber et. al). These findings suggest a potential link between the virus and neurological changes relevant to Parkinsonian disorders, highlighting the need for further investigation into the long-term neurological effects of COVID-19.
Research using human retinal tissue and organoids shows that SARS-CoV-2 induces amyloid-β protein aggregates, a hallmark of Alzheimer’s disease, supporting the hypothesis that amyloid-β acts as an immune response to microbial infections, potentially linking it to neurological symptoms in COVID-19, with reduced aggregation observed upon pharmacological inhibition of neuropilin-1. (Miller et. al).