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01-04-2010, 05:38 PM | #1 | ||
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In Remembrance
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This study compared amyloid load in dementia with lewey bodies [DLB], a very malignant illness, with parkinson's disease w/ dementia [PDD] and normal brains.
J Neurol Neurosurg Psychiatry 2008;79:1331-1338 doi:10.1136/jnnp.2007.127878
Conclusion: This study suggests that amyloid load is significantly raised in over 80% of subjects with DLB, while amyloid pathology is infrequent in PDD. These in vivo PET findings suggest that the presence of amyloid in DLB could contribute to the rapid progression of dementia in this condition and that anti-amyloid strategies may be relevant. http://jnnp.bmj.com/content/79/12/1331.abstract
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paula "Time is not neutral for those who have pd or for those who will get it." |
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01-04-2010, 06:36 PM | #2 | ||
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In Remembrance
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it's harder to understand and there is no abstract. it is current tho so we need to try to get a copy . there doesn't seem to be much research on PDD.
I know there are some who have relatives with pd or maybe you personally who have been helped by Alzheimers drugs. would you please share your experience? i don't want to keep a drug that works away from anyone. but with the track record of the drug industry......... they could be trying to lump the dementias together and create a dementia, gait and postural instability market. they have been working on a DBS for PPN but i just received a pipeline email saying they don't work. when are the patients going to be utilized at the research tables? the right patients, who know a bit about it all? how bad does it have to get? do we have to investigate pd nursing home deaths or near deaths following the addition of AD drugs ? shouldn't all doctors and nursing homes be aware that you just can't prescribe these drugs because they are FDA approved. That whole process needs to be investigated. I'm only one person. we need a friendly medical researcher or movement disorder specialist to come in and talk to us about this. too logical? too easy? too beneath any doctors? too hard and no one knows? the latter i can accept..... the irony is so glaringly evident.....it takes 15 years to get FDA approval for a drug that might help us but quiet approval of a drug that could kill us happened quickly ad globally. what gives? I would love to hear personal experiences with AD drugs and pd patients. we may need something like AD med at the end, but not all of us and certainly not without dementia. the article posted by olsen about anticholinergics causing cognitive decline......amantadine is not a major anticholinergic, but two things stick out with that article:
thanks, paula http://www.springerlink.com/content/...ext.pdf?page=1
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paula "Time is not neutral for those who have pd or for those who will get it." |
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01-04-2010, 07:16 PM | #3 | ||
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Senior Member
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Paula,
I know these are difficult topics for an open forum, but I really think that there must be a clear definition of the different types of dementias out there, that would clarify a lot. If there are people who do know more about this, especially professional people, please post.... Completely by chance and anecdotally I once came across a story of an elderly PD patient who was being treated with Mirapex who was described as having dementia, and his family was 'having a game' dealing with him. He was displaying some of the obsessive compulsive behaviours we know so well in younger patients, along with night-time restlessness and 'fighting' in his sleep. From all accounts he was completely bewildered by it, it was out of character, and otherwise he was intellectually sound - but by then he was in a home and his treatment was out of his families control. Needless to say I have often wondered whether that really was dementia or not....... The potential for problems of over-, under-, and improper medication in disempowered groups of people is a problem that is not going to go away easily - in fact it is only time and a fresh generation of empowered patients that will make a difference, plus some really enlightened medical thinking.... |
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"Thanks for this!" says: | paula_w (01-04-2010) |
01-04-2010, 08:11 PM | #4 | ||
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In Remembrance
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so very well written lindy, and it encompasses everything.....that is a sad story.
keep your intuition and experiences coming. we need just that. paula
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paula "Time is not neutral for those who have pd or for those who will get it." |
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01-04-2010, 10:50 PM | #5 | |||
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This is interesting, too:
May 27, 2009 Mapping of brain acetylcholinesterase alterations in Lewy body disease by PET H. Shimada, MD, S. Hirano, MD, PhD, H. Shinotoh, MD, PhD, Objective: To characterize brain cholinergic deficits in Parkinson disease (PD), PD with dementia (PDD), and dementia with Lewy bodies (DLB). Methods: Participants included 18 patients with PD, 21 patients with PDD/DLB, and 26 healthy controls. The PD group consisted of nine patients with early PD, each with a disease duration of less than 3 years, five of whom were de novo PD patients, and nine patients with advanced PD, each with a disease duration greater than or equal to 3 years. The PDD/DLB group consisted of 10 patients with PDD and 11 patients with DLB. All subjects underwent PET scans with N-[11C]-methyl-4-piperidyl acetate to measure brain acetylcholinesterase (AChE) activity. Brain AChE activity levels were estimated voxel-by-voxel in a three-compartment analysis using the arterial input function, and compared among our subject groups through both voxel-based analysis using the statistical parametric mapping software SPM5 and volume-of-interest analysis. Results: Among patients with PD, AChE activity was significantly decreased in the cerebral cortex and especially in the medial occipital cortex (% reduction compared with the normal mean = –12%) (false discovery rate–corrected p value <0.01). Patients with PDD/DLB, however, had even lower AChE activity in the cerebral cortex (% reduction = –27%) (p < 0.01). There was no significant difference between early PD and advanced PD groups or between DLB and PDD groups in the amount by which regional AChE activity in the brain was reduced. Conclusions: Brain cholinergic dysfunction occurs in the cerebral cortex, especially in the medial occipital cortex. It begins in early Parkinson disease, and is more widespread and profound in both Parkinson disease with dementia and dementia with Lewy bodies. ********************** Cholinergic denervation occurs early in Parkinson disease Nicolaas I. Bohnen and Roger L. Albin Published online before print June 17, 2009 There's no abstract. An earlier article: Cognitive correlates of cortical cholinergic denervation in Parkinson’s disease and parkinsonian dementia Journal Journal of Neurology Publisher Steinkopff ISSN 0340-5354 (Print) 1432-1459 (Online) Issue Volume 253, Number 2 / February, 2006 Abstract We recently reported findings that loss of cortical acetylcholinesterase (AChE) activity is greater in parkinsonian dementia than in Alzheimer’s disease (AD). In this study we determined cognitive correlates of in vivo cortical AChE activity in patients with parkinsonian dementia (PDem, n = 11), Parkinson’s disease without dementia (PD, n = 13), and in normal controls (NC, n = 14) using N–[11C]methyl–piperidin–4–yl propionate ([11C]PMP) AChE positron emission tomography (PET). Cortical AChE activity was significantly reduced in the PDem (–20.9%) and PD (–12.7 %) subjects (P < 0.001) when compared with the control subjects. Analysis of the cognitive data within the patient groups demonstrated that scores on the WAIS-III Digit Span, a test of working memory and attention, had most robust correlation with cortical AChE activity (R = 0.61, p < 0.005). There were also significant correlations between cortical AChE activity and other tests of attentional and executive functions, such as the Trail Making and Stroop Color Word tests. There was no significant correlation between cortical AChE activity and duration of motor disease (R = –0.01, ns) or severity of parkinsonian motor symptoms (R = 0.14, ns). We conclude that cortical cholinergic denervation in PD and parkinsonian dementia is associated with decreased performance on tests of attentional and executive functioning.
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. There are only three colors, 10 digits, and seven notes; it's what we do with them that's important. ~John Rohn |
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"Thanks for this!" says: | paula_w (01-05-2010) |
01-04-2010, 10:57 PM | #6 | |||
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Member
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Our problems are much more complicated than a lack of dopamine...
History of falls in Parkinson disease is associated with reduced cholinergic but not nigrostriatal dopaminergic activity N Bohnen, K Frey, M Muller, R Koeppe, M … - Society of Nuclear …, 2009 - Soc Nuclear Med J Nucl Med. 2009; 50 (Supplement 2):1235 Nicolaas Bohnen1, Kirk Frey1, Martijn Muller1, Robert Koeppe1, Michael Kilbourn1 and Roger Albin2 Conclusions: These data indicate that unlike nigrostriatal dopaminergic denervation, cholinergic hypofunction contributes to increased fall risk in PD. Thalamic AChE activity also had a significant inverse relationship with the absolute number of falls. In this respect, thalamic AChE activity in part represents the cholinergic output or projection area of the brainstem pedunculopontine nucleus (PPN), which is a locomotor nucleus involved in gait control. http://jnumedmtg.snmjournals.org/cgi...Abstracts/1235
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. There are only three colors, 10 digits, and seven notes; it's what we do with them that's important. ~John Rohn |
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"Thanks for this!" says: | paula_w (01-05-2010) |
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