Severe Canine Demodicosis Induces Neurological Impairment through Cutaneo-Cerebral Axis Activation

Canine demodicosis, caused by infestation with the mite Demodex canis, is a common dermatopathy with the potential for systemic progression. While immunosuppressive mechanisms involving interleukin-۱۰ (IL-۱۰) upregulation and tumor necrosis factor-alpha (TNF-α) suppression have been documented, the associated neuropathological consequences and underlying neuroimmune mechanisms remain inadequately characterized. This study employed integrated behavioral assessments, neurochemical profiling, and immunological analyses to investigate the neurological sequelae in advanced demodicosis. The methodology encompassed cognitive-motor function testing, quantification of acetylcholinesterase activity, and serum cytokine profiling. Our findings clearly demonstrate that severe Demodex canis infestation induces significant cognitive deterioration, memory impairment, and motor incoordination. Mechanistically, mite-induced cutaneous inflammation triggers an elevation in IL-۱۰ and suppression of TNF-α. This cytokine shift leads to a systemic upregulation of acetylcholinesterase. The subsequent hyperactivity of this enzyme, in turn, causes a central depletion of acetylcholine, a neurotransmitter vital for learning, memory, and motor coordination. This cascade of events establishes a direct causal link between cutaneous inflammation and central nervous system dysfunction. This study provides novel evidence for the involvement of a "Cutaneo-Cerebral Axis" in the pathogenesis of demodicosis. These findings redefine severe demodicosis as a "neuro-immuno-cutaneous" disorder. Understanding this novel axis paves the way for new therapeutic strategies. These approaches could focus on the targeted modulation of this axis through interventions addressing both the skin inflammation and its neurological consequences. Such therapies might include selective cytokine modulators, peripherally-acting acetylcholinesterase inhibitors, or neuroprotective agents. In summary, this research expands our conceptual framework from a purely dermatological condition to a more complex disorder with systemic and neurological manifestations, emphasizing the need for a multifaceted therapeutic approach.

کلیدواژه ها:

Canine demodicosis ، Cutaneo-Cerebral Axis ، Neurological impairment ، Acetylcholinesterase ، Interleukin-۱۰