1. Gerontology. 1987;33(3-4):168-71.

Dopamine action and disorders of neurotransmitter balance.

Birkmayer W, Birkmayer JD.

Evangelic Hospital, Vienna, Austria.

Disorders of neurotransmitter balance are observed in Parkinson's disease,
pharmacotoxic psychosis and depression. The dopamine-serotonin ratio is reduced
to about 20% in Parkinson and pharmacotoxic patients in the caudate nucleus and
in the substantia nigra. The serotonin content in these brain areas is lowered
only to about 50% in comparison to that of the control, whereas the dopamine
level is reduced to 85% in Parkinson patients. This dopamine deficiency has been
substituted by exogenous supply of L-dopa in combination with decarboxylase and
monoaminooxydase inhibitors. First evidence is presented that L-dopa can be
replaced, at least partially, by iron in form of a ferriascorbate complex. This
iron compound improves the symptoms of Parkinson's disease to almost the same
extent as L-dopa.

PMID: 3653699 [PubMed - indexed for MEDLINE]

The Birkmayers were once big names in PD research. Here they report that iron is as good as Ldopa. When we ask about iron we get vague warnings and little more. Anyone know more on this?

I just realized that I had posted on this about three weeks ago but rather than erase it, I think it needs attention.
The Birkmayers (W & JD) were German. I suspect that W was father and JD son because W has 172 papers to his credit at PubMed. JD has just two - the one you read here and a companion one published the same year. W , with his 172 papers, built up a larger body of work. But these two papers were numbers 162 and 163. His career was just about over, whether he knew it or not.

So what happened to the Birkmeyers?

I spoke with Dr. Birkmeyer on the phone in '94. He told me CAT scans were pointless (unless I was having headaches or other unique sx diff than pd sx)and that I should take NADH (i think he had the patent or had s ome interest in NADH). it was a very short conversation!

md

http://www.webs.uidaho.edu/wisui/Kau...lar%20Iron.pdf

I didn't have the stamina to read the above long article which may shed light on the subject.

Interestingly, my blood test done after starting sinemet showed deficiency in iron and my family doctor perscribed iron tablets which I took for one month.

I always assumed that iron increases oxidative stress. but I realise now that iron is vital and it is delicately kept in balance by the cell.

Imad

Hi Rick,
We PDers have abnormal iron levels, abnomally high that is, up to 7 times normal. iron is a powerful oxidation catalyst, so it seems not a good idea to add more.See

http://www.sciencedaily.com/releases...0610081311.htm
Science News Share Blog Cite Print Bookmark Email
Parkinson's Disease Linked To High Iron Intake
ScienceDaily (June 10, 2003) — ST. PAUL, MN – People with high levels of iron in their diet are more likely to develop Parkinson's disease, according to a study in the June 10 issue of Neurology,


http://www.physorg.com/news169899879.html
Parkinson's disease: Iron accumulation to the point of demise


Multiple studies implicate iron in the pathophysiology of Parkinson's disease (PD). In the brains of patients with PD, iron levels are elevated and the levels of iron-binding proteins are abnormal. Iron has been suspected to contribute to PD because Fe(II) is known to promote oxidative damage. Recent studies suggest that an additional mechanism by which iron might contribute to PD is by inducing aggregation of the alpha-synuclein, which is a protein that accumulates in Lewy bodies in PD.

PMID: 11843096 [PubMed - indexed for MEDLINE]

Might be an idea to contact the Birkmeyers if they are still around.

Ron

1. Int J Alzheimers Dis. 2010 Dec 27;2011:720658.

Iron and mechanisms of neurotoxicity.

Salvador GA, Uranga RM, Giusto NM.

Instituto de Investigaciones Bioquímicas Bahía Blanca, Universidad Nacional del
Sur y Consejo Nacional de Investigaciones Científicas y Técnicas, 8000 Bahía
Blanca, Argentina.

The accumulation of transition metals (e.g., copper, zinc, and iron) and the
dysregulation of their metabolism are a hallmark in the pathogenesis of several
neurodegenerative diseases. This paper will be focused on the mechanism of
neurotoxicity mediated by iron. This metal progressively accumulates in the brain
both during normal aging and neurodegenerative processes. High iron
concentrations in the brain have been consistently observed in Alzheimer's (AD)
and Parkinson's (PD) diseases. In this connection, metalloneurobiology has become
extremely important in establishing the role of iron in the onset and progression
of neurodegenerative diseases. Neurons have developed several protective
mechanisms against oxidative stress, among them, the activation of cellular
signaling pathways. The final response will depend on the identity, intensity,
and persistence of the oxidative insult. The characterization of the mechanisms
mediating the effects of iron-induced increase in neuronal dysfunction and death
is central to understanding the pathology of a number of neurodegenerative
disorders.


PMCID: PMC3014724
PMID: 21234369 [PubMed - in process]

Interesting thread - I was dx as anemic as a young child and was given desicated liver pills. Is anemmia a common pattern inearly onsetttters?

I would suspect I should eat liver as a dietary regimen but what kind?

I have a repetitive dream of getting trapped at the iron works steel mill plant in the town where I grrew up in.

md

Everything that is good in the right place and time has the potential to be deadly in the wrong setting. The BBB plays a central role in this compartamentalization. An intact BBB allows a high level of iron or anything else to exist in blood and muscle while maintaining a different level in the CNS. Trouble comes with the failure of this system.


1. J Neurochem. 2010 Dec 7. doi: 10.1111/j.1471-4159.2010.07132.x. [Epub ahead of
print]

The relevance of iron in the pathogenesis of Parkinson's disease.

Sian-Hülsmann J, Mandel S, Youdim MB, Riederer P.

Clinical Neurochemistry, National Parkinson Foundation Centre of Excellence
Laboratories, Clinic and Polyclinic for Psychiatry, Psychosomatic and
Psychotherapy, Medical School, University of Würzburg, Würzburg, Germany Eve Topf
Centre of Excellence for Neurodegenerative diseases, Technion-Rappaport Faculty
of Medicine, Haifa, Israel Department of Biology, World Central Yonsei
University, Seoul, South Korea.

J. Neurochem. (2011) 10.1111/j.1471-4159.2010.07132.x ABSTRACT: Alterations of
iron levels in the brain has been observed and documented in a number of
neurodegenerative disorders including Parkinson's disease (PD). The elevated
nigral iron levels observed in PD may reflect a dysfunction of brain iron
homeostasis. Under normal physiological conditions excess iron can be
sequestrated in ferritin and neuromelanin. Alternatively, the excess iron may
represent a component of brain iron deposition associated with ageing. The
aetiology of idiopathic PD largely remains an enigma. However, intensive
investigations have provided a host of putative mechanisms that might contribute
to the pathogenesis underlying the characteristic degeneration of the
dopaminergic neurons in the substantia nigra (SN). The mechanisms proposed
include oxidative (and nitrative) stress, inflammation, excitotoxicity,
mitochondrial dysfunction, altered proteolysis and finally apoptotic induced cell
death. Iron-mediated cellular destruction is mediated primarily via reactive
oxygen or/and nitrogen species induced oxidative stress. Furthermore, these
pathogenic mechanisms appear to be closely interlinked to the cascade of events
leading to cellular death. There are conflicting reports about the stage during
disease progression at which nigral iron change occurs in PD. Some have found
that there are no changes in iron content SN in asymptomatic incidental Lewy body
disease, suggesting it may represent a secondary event in the cascade of neuronal
degeneration. In contrast, others have found an elevation of iron in SN in
pre-clinical stages. These discrepancies may be attributed to the occurrence of
different sub-groups of the disease. This concurs with the notion that PD
represents a group of related diseases with a number of potential pathogenic
pathways.


PMID: 21138437 [PubMed - as supplied by publisher]