Parkinson's, Lewy body dementia and Alzheimer's Pathology

Recent research has revealed that changes in sebum — the natural oil your skin produces — can appear years before Parkinson’s symptoms (Marsh). Two diagnostic tests under development use sebum to help detect the disease (Uehara et. al) (Robinson). And what feeds on sebum? Microscopic skin mites (El-Moamly et. al).

The Evidence

• Sebum in Parkinson’s: PD patients produce more sebum early, even before tremors begin (Paz et. al).
• Mite Biology: Demodex mites live in hair follicles and oil glands, feeding on sebum (Cleveland Clinic). The global prevalence of the Demodex Mite is approximately 35% based on studies (Maleki et.al).
• Lindane Study: A nationwide study found people treated with lindane — a mite-killing pesticide — had a significantly lower risk of Parkinson’s (Tsai et. al). 
• Skin Disorders & PD: "Seborrheic dermatitis is considered to occur as a premotor feature of Parkinson’s disease referable to dysregulation of the autonomic nervous system.” (Ravn et. al) Seborrheic dermatitis and rosacea (conditions linked to mites (Ungex)(Karabay et. al)) are more common in PD (Karingaoclu et. al) (Zhao et. al).   Conditions like seborrheic dermatitis (prevalent in 52-59% of PD patients vs. 3% in the general population)(Ravn et. al) and rosacea (linked to Demodex mites(Karabay et. al)) are associated with higher risks of PD (2-fold) and AD (28% increased in women)(National Rosacea Society)(Egeberg et. al). Demodicosis in Humans- "Rosacea, an infectious disease: why rosacea with papulopustules should be considered a demodicosis. A Narrative review" (Forton) The Syn-One test, which uses skin biopsies to detect phosphorylated alpha-synuclein, a potential precursor to Lewy bodies, may aid in diagnosing neurodegenerative diseases(Mitchell). However, it cannot distinguish between Parkinson’s disease, Lewy body dementia, or Shy-Drager Syndrome (Multiple System Atrophy) (Mitchell). The study found that phosphorylated α-synuclein (P-SYN) was not detected in all skin biopsies, with positivity rates varying by body region (Mitchell).
• Inflammation and Immune Response: Specific Demodex components activates TLR-2 receptors (El-Moamly et. al).TLR-2 receptors promote neuroinflammation as seen in AD (Kim et. al) and PD (Dzamko et. al). Beta-amyloid in AD may act as an antimicrobial response to invaders like those carried by mites. House dust mite-induced asthma exacerbates AD by increasing amyloid beta accumulation and neuroinflammation in a mouse model. (Sahu et. al)
• Neurotoxins and Symptoms: Some mites inject neurotoxins via saliva(Glosner et. al). Neurotoxins may disrupt nerve function, leading to movement disorders, memory loss, and cognitive decline—symptoms common in PD, AD, and LBD.
• Mites as Carriers of Pathogens and Prions: Some studies suggest that mites can harbor prions (as shown in lab studies with hay mites and scrapie in animals) (Lupi). Mites are associated with bacteria like Borrelia burgdorferi (Netusil et. al) which is linked to AD (Miklossy et. al) and PD (Knox). This raises the possibility of horizontal transmission to humans, potentially influencing protein aggregates in diseases like AD (beta-amyloid) and PD (alpha-synuclein). 

The Hypothesis
Could chronic mite activity and the microbes they carry influence inflammation, contribute to  Alzheimer's Disease and alter sebum chemistry, and contribute to alpha-synuclein misfolding — a hallmark of Parkinson’s? Further research is needed to explore this hypothesis.

Why This Matters
Understanding the role of mites could open new doors for prevention, earlier diagnosis, and even new treatments.

What’s Next

• Ongoing and needed research

Call to Action:

Raise awareness about this hypothesis by discussing it with healthcare professionals or researchers. Support calls for further studies to explore these potential connections.  

These connections underscore the hypothesis that mites could be an underexplored environmental trigger. However, this is based on observational and hypothetical links—further research is essential to validate or refute them.

Disclaimer: This article presents a hypothesis based on personal observations and limited studies, not definitive evidence. It is not intended as medical or veterinary advice. Always consult licensed medical or veterinary professionals for diagnosis and treatment. The author has no affiliation with any testing services or medical practices.

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).