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PARKINSON'S DISEASE
Congresso Società Italiana di Neurologia (SIN) - Cernobbio (Co) Ottobre 2005
Fiore D.
Indipendent Professional
Piove di Sacco (PD) - Italia
Objective: Etiopathogenesis - Treatment
| Attenzione.
Il meccanismo della depigmentazione neuronale, descritto in questa versione,
non è stato confermato dalle ricerche successive. La patogenesi (la spiegazione più probabile), coerente con
la Biologia Molecolare, è descritta nella versione gennaio 2007, cui si rimanda. |
Subjects - Methods - Results.
In seven patients out of seven with defined Parkinson's disease and in one in which Parkinson's has been diagnosed and, ten years later, Amyotrophic Lateral Sclerosis, the research of the anti Bordetella antibodies resulted positive for infections in progress.
Discussion:
Melanin is constituted of dopamine which, copolymerising with cyclical groups containing sulphur, forms "granules of insoluble protein pigment" (melanosomes); the neuromelanin, contained in the pigmented neurons, is melanin polymer incorporated in a glycolipid matrix. In the histological examination: in Parkinsonian midbrains, around the neurons, there is an insoluble protein pigment resistant to proteases.
Since the neuromelanin is a melanin polymer we must expect that, in the neurons, the neuromelanin has a physiological role as a "deposit" of ready dopamine (for use when needed, without having to be synthesised when the need arises). The identity of the chemical-physical structure of the melanin and of the neuromelanin shows that the pigmented neurons of the Substantia Nigra (SN) phagocytize from outside the melanin and incorporate it into a glycolipid matrix. The role as a "deposit of ready to use dopamine" also explains why neuromelanin deposits only in the cells that use the dopamine as a neurotransmitter, and not in all the neurons of the SNC.
In a Bordetelle toxin infection:
- The Pertussis Toxin: fixing to the neuroepithelia, it mechanically hinders entry of the melanosomes into the cell; ADP-ribosylating the Protein G-inhibitor first prevents the repair of small breaks in the DNA, then it activates the neuronal apoptosis; activating the Phospholipase produces "eicosanoids" and intervenes in the biosynthesis and deactivation of the "endogen endocannabinoids".
- The Pertussis Adenylatecyclase, fixing to the GM1, mechanically hinders entry of the melanosomes into the cell; by an unknown mechanism, it inhibits phagocytosis.
- The Cytotracheal Toxin inhibiting the ATPase, prevents the use of the energy (ATP <-> ADP) and transmembrane ionic exchange.
- The Pillemer Factor irreversibly fixes to the "stroma" (cytoskeletons) of the neuroepithelia.
Conclusions
In Parkinson's disease:
- first, absorption of the melanosomes and the self-assembly of the intra-cellular neuromelanin is prevented (depigmentation of the SN neurons and dopamine deficiency);
- then, the death of the intoxicated neurons eventually follows (neuronal impoverishment) and the formation of the "Lewy Bodies" (masses of filaments of the cytoskeleton, antigenically different from the neurofibrillary degeneration of Alzheimer).
Treatment: Long-term Erythrocyn®.
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