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Bev Steward wrote in part: >Knowing what we do now about the brain being 80% damaged already >when the first symptoms become noticable, I can trace several times >in my life when I ran extremely high temperatures (105.8 & 106 >degrees F)) with bouts of pneumonia, double pneumonia, infection and >measles (at age 30). Encephalitis comes with high fevers, so I >postulate that those fevers could have burned out cells in my >substantia nigra. > >So, you can see why I agree with doing research in this direction. I >wonder if it might lead to understanding why more people under 50 are >being diagnosed as having PD. My personal thanks to Bill Langston >and his crew! i have an unusual insight regarding this possibility. it comes from my career as a solid propulsion rocket scientist/engineer. My solid propellant rocket experience included some failure investigation research that determined that dark inclusions in translucent doublebase propellant grains cause abnormal combustion. The flame zone normally exists just above the regressing surface and is radiating heat with temperature and pressure elevated. The regression of the surface is uniform unless the portion of radiation passing through the unburned propellant is not uniformly absorbed. Dark or opaque propellant or inclusions get warmer. At times, burning initiates in subsurface hot spots resulting in overpressurization rocket case rupture. I am curious if the darkness of the substantia nigra is a variable amongst individuals with significance in radiation absorption. Dr. Jeffrey Tosk reported photon-phonon measurements which seem to add credence to the possibility. It may be that the energy increase of the blacker loci is the proximate cause of some overactivity during feverish illness that damages the neurons sufficiently to induce apoptosis. It seems easy enough to make some sort of measurements of sunlight exposure on animal cadavers perhaps. pathologists observations relevant to substancia nigra damage and coloration of PD patients and fever-including lethal diseases might provide clues that validate or deny any such energy concentration due to pigment. I wonder if there is any test or measurement that can be done to ascertain if the conjecture that I have "toyed" with might be shown as pertinent - or not. The concept is somewhat related to the light sensitivity of the brain. I have Parkinson's disease. One aspect of this is change in the blackest portion of the brain, the substantia nigra. I know from numerous translucent solid propellant rocket motor propellant investigations of abnormal burning front progression - that the translucent or transparent propellant can be heated in loci which are contaminated with dark inclusions which absorb more of the radiant light energy; then, rise in temperature. The temperature rise can be nominal such that the portion heated is warm and burns at a higher rate because of this - or, in some instances, the localized heating is quite significant and actually causes ignition of the heated portion - which will often cause pressure vessel rupture - id est, the rocket bursts apart violently. The amount of radiant energy entering the brain is not known to me. However, the substantia nigra being darkest might be warmest - which would increase chemical activity. The Lewy bodies and neuromelanin are not something I am visually acquainted with. In fact, I am unsure what the normal substantia coloration is at birth, during development that is normal and development of Parkinsonism. I think I have heard that the substantia becomes whitened with disease, but I also remember reading that dopamine gets combined into neuromelanin as part of the disease. Is not neuromelanin black? ****** excerpted from: Zinc in pigmented cells and structures, interactions and possible roles Jan Borovansk? Observations of Prota and his associates have recently revived attention to the role of zinc in biosynthesis of melanins. They observed that various transition metals including Zn2+ affected markedly the chemical properties of melanin formed by the tyrosinase-catalyzed oxidation of L-dopa by increasing the incorporation of 5,6-dihydroxyindole-2-carboxylic acid into the pigment polymer [67,68]. Zn2+ can thus imitate function of dopachrome oxidoreductase. When acting together the inhibition of 5,6-dihydroxyindole-2-carboxylic acid decarboxylation was greater than that produced by Zn2+ or dopachrome oxidoreductase separately [50]. The suggestion that the presence of carboxylated indole units in natural melanins is due to the intervention in the melanogenesis of metal ions can be accepted. However, the role of Zn2+ namely in this respect appears to be uncertain because the free Zn2+ cation is damaging to biological systems and thus is associated with other molecules as Zn-ligand complex (see the section 3) resulting in a actual free Zn2+ ion concentration that is 10-3 - 10-6 that of the total zinc concentration [8,98]. Whether Zn2+-ligand complexes can influence melanogenesis it has not been tested. Zn2+ ions were shown to inhibit the initial rate-limiting reaction of melanogenesis - tyrosine hydroxylation and thus to have a role in the regulation of melanogenesis [50]. The frequent occurence of necroses in melanoma tissue [13] and the presence of H2O2 [24] make the metal driven free radical processes in pigmented tumours probable. Moreover, increased malondialdehyde levels found in the livers of B16 and S91 melanoma-bearing mice [13,71] suggest that the tumours alter host antioxidant defenses. Alteration of iron metabolism and increased levels of lipid peroxidation are characteristic of substantia nigra in Parkinson's disease [30] and the fact that also zinc levels in substantia nigra are markedly increased under these circumstances may indicate a physiological response to oxidative stress [29]. Evidence documenting that a number of catecholic melanin precursors, including cysteinyldopas and dihydroxyindoles, are photochemically unstable in vitro in the presence of biologically relevant ultraviolet radiation was presented by Koch and Chedekel [52]. Definitive evidence of occurrence of these reactions in vivo is currently unavailable, nevertheless these photochemical processes are expected to have a role in the pathogenesis of various pathological processes. The high level of zinc in epidermal and eye pigment cells may again indicate a physiological defense against the potential danger of oxidative stress. ******** Some aspects of this disease are undoubtedly tied to the de-pigmentation. I have not any reference information on the autopsy findings. does anyone have such a thing as a source of some detail? some questions and conjectures: Does the substantia nigra have the dark pigmentation in the fetus? or does the pigmentation develop after birth? Have we measured the amount of light in the brain? I doubt that 'no' light enters. Visible light might not be plentiful, nor other wavelengths of electromagnetic radiation, but there must be quite a lot of cumulative energy since some wavelengths of radiation pass through readily. Even if the level of radiation is low, the black portion will tend to absorb - and become warmer. Such warmth might accelerate activity and/or reactivity. Degradation might accelerate as darkening increases. It seems easy enough to make some sort of measurements of sunlight exposure on animal cadavers perhaps. pathologists observations relevant to substancia nigra damage and coloration of PD patients and fever-including lethal diseases might provide clues that validate or deny any such energy concentration due to pigment. I wonder if there is any test or measurement that can be done to ascertain if the conjecture that I have "toyed" with might be shown as pertinent - or not. The concept is somewhat related to the light sensitivity of the brain. I have Parkinson's disease. One aspect of this is change in the blackest portion of the brain, the substantia nigra. I know from numerous translucent solid propellant rocket motor propellant investigations of abnormal burning front progression - that the translucent or transparent propellant can be heated in loci which are contaminated with dark inclusions which absorb more of the radiant light energy; then, rise in temperature. The temperature rise can be nominal such that the portion heated is warm and burns at a higher rate because of this - or, in some instances, the localized heating is quite significant and actually causes ignition of the heated portion - which will often cause pressure vessel rupture - id est, the rocket bursts apart violently. The amount of radiant energy entering the brain is not known to me. However, the substantia nigra being darkest might be warmest - which would increase chemical activity. The Lewy bodies and neuromelanin are not something I am visually acquainted with. In fact, I am unsure what the normal substantia coloration is at birth, during development that is normal and development of Parkinsonism. I think I have heard that the substantia becomes whitened with disease, but I also remember reading that dopamine gets combined into neuromelanin as part of the disease. Is not neuromelanin black? guess i am wanting to learn more - to see if this approach has some merit. my encounter with typhoid fever at the age of 11 may have done me some damage. responses welcome; sincerely, ron Ronald Vetter 1936, dz PD 1984, carbidopa/levodopa, Mirapex, selegiline [log in to unmask] Ridgecrest, California http://www.ridgecrest.ca.us/~rfvetter