View Single Post
Old 10-29-2007, 03:07 PM
reverett123's Avatar
reverett123 reverett123 is offline
In Remembrance
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
reverett123 reverett123 is offline
In Remembrance
reverett123's Avatar
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
Default Sorry to rain on the parade. but...

...this should be old news to every researcher and doctor in the world as the paper below shows. Thirty dam*** years ago. My point is that people have to get noisy about this at every opportunity.

1: Natl Inst Drug Abuse Res Monogr Ser. 1975 Nov;(3):13-21.

Brain monoamines and parkinsonism.

Hornykiewicz O.

In Parkinson's disease there is a derangement of the metabolism of at least 3
major brain monoamines, namely, dopamine (DA), norepinephrine (NE) and serotonin
(5-HT). Of these alterations the severe deficiency of DA in the striatum is most
characteristic, being (a) found in Parkinsonian syndromes of any etiology and (b)
significantly correlated with the degree of cell loss in the substantia nigra,
and the severity of the main symptoms. On the basis of neurochemical-clinical
correlations Parkinson's disease may be subdivided into (a) an asymptomatic stage
during which the striatal DA deficiency may reach a marked degree but can be
compensated by the remaining DA neurons, and (b) the stage of decompensation
(i.e. clinically manifest disease) which ensues when the depetion of striatal DA
reaches 70% or more. L-Dopa's main feature as a specific antiparkinson drug may
be seen in its potential to revert the decompensated stage of the disease to the
stage of functional compensation. This is in many cases possible because (a) the
DA turnover in the remaining DA neurons is increased, providing for a high rate
of formation (from L-dopa) and release of DA; (b) the "denervated" striatal
receptors are supersensitive to DA; and (c) the newly-formed DA can be expected
to reach a wide area of the striatum due to the high degree of divergence of the
dopaminergic innervation. Compared with the striatal DA deficiency, the degree of
NE and 5-HT decrease in the Parkinsonian brain is moderate. The decrease in NE
may be due to the (moderate) cell loss in the locus coeruleus; at present no
morphological basis for the lowering of brain 5-HT is known. The functional
significance of the changes in brain NE may be an aggravation of akinesia. The
decrease in brain 5-HT may be related to aspects of Parkinson's disease in turn
related to affective behavior and mood.

PMID: 787796 [PubMed - indexed for MEDLINE]
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
reverett123 is offline   Reply With QuoteReply With Quote