I decided that it was time to simply post some articles for people who wanted to know more about the disease, and what the latest research was telling us. So, below you'll find a couple of articles from the Lewy Body Dementia Assn, which I thought to be of interest - perhaps a little clinical, but they do give a much better idea of who is at risk at becoming a patient, and what the latest findings are.
I had no idea, either, there was an Alzheimer's Gene....
Remember, LBD is still an enigma, but they're discovering more about this form of dementia, which is the second leading cause of dementia after Alzheimer's!
- See more at: http://www.lbda.org/content/elevated-blood-lipids-increase-risk-dementia-parkinsons#sthash.ra2iGHXr.dpuf
- See more at: http://www.lbda.org/content/alzheimer-gene-increases-risk-of-lewy-body-dementias#sthash.RdNz2EDu.dpuf
I had no idea, either, there was an Alzheimer's Gene....
Remember, LBD is still an enigma, but they're discovering more about this form of dementia, which is the second leading cause of dementia after Alzheimer's!
ELEVATED BLOOD LIPIDS INCREASE RISK OF DEMENTIA IN PARKINSON’S
GBA is a genetic variation that is associated with sporadic Parkinson’s disease and severe cognitive impairment and is also associated with dementia with Lewy bodies. Approximately 4-7% of people with Parkinson’s carry this genetic variation. Research into GBA in Parkinson’s has helped researchers identify markers in the blood that may indicate which people with Parkinson’s are at risk for cognitive impairment and dementia even if they don’t have the GBA variant.
GBA changes how certain fats in the blood (lipids, ceramides and glucosylceramides) are metabolized. People with Parkinson’s another disease caused by and the GBA variation, Gaucher’s disease, have higher levels of these fats in their blood. Researchers recently discovered that Parkinson’s patients who not have the GBA variation also have higher levels of these fats and are more likely to have cognitive impairment and dementia. There are currently no tests available to identify which people with Parkinson’s will progress to dementia.
Michelle M. Mielke, PhD, and researchers from the US and Germany studied the blood of 26 cognitively normal people with Parkinson’s disease, 26 people with Parkinson’s and cognitive impairment or dementia, and 5 cognitively normal, healthy controls. The healthy controls had the lowest levels of these lipids, followed by those with Parkinson’s disease but no cognitive impairment. People with Parkinson’s disease and some degree of cognitive impairment or dementia had the highest levels of these fats. Cognitive impairment was not associated with other blood lipids like LDL or HDL cholesterol or triglycerides.
These results suggest the importance of the metabolism of certain blood fats in the underlying disease process of Parkinson’s disease. While this study was small in size and will need to be replicated in larger studies to confirm the findings, blood tests could someday predict which people with Parkinson’s will progress to dementia.
In 2012, LBDA and the Alzheimer’s Drug Discovery Foundation awarded Dr. Mielke and Dr. Rodolfo Savica a grant to explore how blood lipid markers are associated with brain pathology of Lewy body dementias. This research will further clarify the potential of blood lipids to serve as a possible clinical biomarker for Lewy body dementias.
This study was first published online Sept. 18 in the journal PLoS One.
Citation: Mielke MM, Maetzler W, Haughey NJ, Bandaru VVR, Savica R, Deuschle C, Gasser T, Hauser AK, Gräber-Sultan S, Schleicher E, Berg D, Liepelt-Scarfone I. Plasma ceramide and glucosylceramide metabolism is altered in sporadic Parkinson’s disease and associated with cognitive impairment: a pilot study. PLoS ONE 2013;Sept 18;8(9):e73094.
"ALZHEIMER GENE" INCREASES RISK OF LEWY BODY DEMENTIAS
Lewy body disease is the underlying biological process in the brain associated with Lewy body dementia and Parkinson’s disease. While Lewy body disease can exist in a "pure" form with little or no co-existing Alzheimer’s disease, at least half of individuals with Lewy body disease also have significant amounts of Alzheimer’s pathology.
Until now, research has not revealed why people can possess the pathological hallmarks of one or both diseases. However, a new study has revealed that a genetic variant previously known to increase the risk of developing both early-onset and late-onset Alzheimer’s disease is also a risk factor for Lewy body dementias.
The study, led by Debby Tsuang, M.D., Professor of Psychiatry and Behavioral Sciences at the University of Washington and Veterans Affairs Puget Sound Health Care System (VAPSHCS), included 640 people with dementia and 269 healthy individuals and included autopsies on all participants. Clinical and neuropathological assessments resulted in the following dementia categorizations:
| Category | No. of People |
| Parkinson’s Disease Dementia (PDD) | 81 |
| Pure Dementia with Lewy Bodies (pDLB) | 91 |
| Co-existing Alzheimer’s Disease and Lewy Body Disease (LBD-AD) | 224 |
| Alzheimer’s Disease (AD) | 244 |
| Healthy Controls | 269 |
After adjusting for age and sex, and using the healthy controls as a reference group, the APOE variant was strongly associated with all four forms of dementia:
- 10-fold increase in the risk of pure Alzheimer’s
- 13-fold increase in the risk of Alzheimer’s with Lewy bodies
- 6-fold increase in the risk of pure Lewy body dementia
- 3-fold increase in the risk of Parkinson’s dementia
Senior author Cyrus P. Zabetian, M.D., Associate Professor of Neurology at the University of Washington and VAPSHCS stated, “APOE ɛ4 is the first genetic risk factor we know of that is shared among AD, pure DLB, and PDD. That indicates that these three diseases might also share some of the same root causes. If this proves to be true, it gives us hope that future therapies aimed at one of these diseases could be effective in treating the others.”
While the APOE variant is a well-established risk factor for Alzheimer’s disease, analysis showed an association between pDLB and PDD which was unexpected. In humans this variant is thought to accelerate the accumulation of amyloid protein. Toxic buildup of amyloid ultimately leads to the development of Alzheimer’s "plaques" and neurodegeneration. In this study, however, the absence of Alzheimer’s pathology in individuals with Lewy body disease indicates the possibility that this genetic variant may influence neurodegeneration through other pathways.
Another implication of the study is that APOE might play a role in determining whether someone with Lewy body disease is diagnosed with DLB or PDD. DLB is diagnosed when dementia occurs before or concurrently with parkinsonism, whereas in PDD, parkinsonism precedes dementia by at least one year. Findings from the study suggest that individuals with Lewy body disease who have the APOE variant are more likely to experience dementia first and thus to be diagnosed with DLB rather than PDD.
Members of LBDA’s Scientific Advisory Council who collaborated on this study include Debby Tsuang, M.D., James B. Leverenz, M.D., Oscar Lopez, M.D., Daniel Weintraub, M.D., Doug Galasko, M.D., and Cyrus P. Zabetian, M.D. The study was first published online on November 19, 2012 in Archives of Neurology and was funded by grants from the Department of Veteran’s Affairs and the National Institutes of Health.
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