Helminthic therapy and neurodegenerative diseases

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    Neurodegenerative disease is a result of the progressive loss of structure or function of neurons, potentially leading ultimately to cell death.

    Neurodegenerative diseases include Multiple sclerosis (MS), Amyotrophic lateral sclerosis (ALS), also known as motor neuron disease / motor neurone disease (MND) and Lou Gehrig's disease, Alzheimer's disease, Parkinson's disease, Dementia with Lewy bodies, Huntington's disease, Multiple system atrophy (MSA), Prion diseases.

    Introduction[edit | edit source]

    The potential for helminthic therapy to help in addressing neurodegenerative disease can be seen most strikingly in multiple sclerosis, which responds extremely well to the presence of helminths. See Helminthic therapy and multiple sclerosis (MS)

    There are also indications that helminths may help in both treating and preventing Parkinson's disease, Alzheimer and dementia.

    A 2019 review paper in the journal, Neuropsychiatry[1], suggested that helminthic therapy may have value in treating other neurodegenerative diseases.

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    Although the molecular mechanism of synaptic damage and neuronal loss in Alzheimer’s disease (AD), Parkinson’s disease dementia (PD) and Lewy body dementia (LBD), frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is poorly understood and differ among different types of neurodegenerative processes, however, the presence of neuroinflammation is a common feature of all these dementia. In the advanced stage of neurodegenerative diseases of the late onset, both innate and adaptive immunity are key determinants of the progression of clinical symptoms of neurodegeneration. Therefore, it can be suggested that immunomodulation of chronic inflammation along with attenuation of humoral and cellular autoimmune reactions may be a universal strategy aimed at suppressing the progression of clinical symptoms and improving the current neuronal function in various neurodegenerative diseases. A promising direction for the development of symptomatic neurodegenerative therapy may be the use of immunomodulatory capabilities of our “old” friends” - parasitic worms and intestinal microflora. Both intestinal bacteria and parasitic worms have evolved together with the immune system of mammals for millennia and have become equisitely powerful immunomodulators, capable of altering and suppressing host immune responses, contributing to slow down excessive inflammatory and autoimmune responses. More recent studies also show that the interaction between intestinal parasites and intestinal microflora significantly changes their immunomodulatory capacity; microflora help helminths modulate host immunity. Presumably human lymphocytes after the ex vivo cultures in the presence of intestinal parasites and gut microbiota (“ménage à trois” system) will be more beneficial for the treatment of patients with dementia. Undoubtedly, many basic and preclinical studies must precede the development of procedures and recommendations for the treatment of late-onset neurodegeneration in humans with the help of parasitic worms and intestinal microflora. It seems, however, that this can be a very promising universal therapy, as the dysregulation of inflammatory and autoimmune reactions is significantly present in various neurodegenerative diseases.

    Scientific papers[edit | edit source]

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    The present study revealed for the first time that the parasite-derived ESPs alleviate gut microbiota dysbiosis and improve cognitive impairment induced by a high-fat diet. This finding suggests that parasite-derived molecules may be used to explore novel drug candidates against obesity-associated neurodegenerative diseases.
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    We find that the outcome of H. polygyrus-dependent immunoregulation is different in healthy, control mice than in mice with existing LPS-induced inflammation. Infection with H. polygyrus protected control mice from some neurodegenerative changes in the brain and reduced depression symptoms, typical for ageing mice. In mice with LPS-induced inflammation and infected with the parasite, the neurodegenerative changes are accompanied by poorer scores of depression, and these were also present in genetically predisposed APPSWE mice.
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    We present evidence that the E4 allele, often associated with cognitive decline, AD, and CVD in industrialized populations with minimal parasite burden, was associated with higher cognitive function among Tsimane Amerindians, but only among individuals with evidence of high parasite burden.

    See also

    APOE4 & the Tsimane study

    Inflammation hypothesis

    Microbiota-gut-brain axis dysregulation

    Autoimmune hypothesis

    IL4

    Prion Paradigm

    Alzheimer's disease[edit | edit source]

    See the scientific papers section, above.

    See also (not directly related) :

    To be linked to the Helminths and SPION study[4] and the fact Helminths could restore the blood-brain barrier.

    Amyotrophic lateral sclerosis (ALS)[edit | edit source]

    See also

    Creutzfeldt–Jakob disease[edit | edit source]

    See Helminths and prion diseases

    Dementia[edit | edit source]

    There is one tentatively positive report of benefit in dementia.

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    I am currently helping someone with dementia. She has been taking NA for one year and whilst we have nothing remotely scientific, her doctors and her husband are pleased that she has not declined and may have some improvements. Early days. [5]

    Huntington's disease[edit | edit source]

    Multiple sclerosis[edit | edit source]

    See Helminthic therapy and multiple sclerosis (MS)

    Parkinson's disease[edit | edit source]

    See Helminthic therapy and Parkinson's disease

    Post-traumatic brain injury[edit | edit source]

    See also

    See also[edit | edit source]