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