Could you compare and contrast Alzheimer’s Disease, Dementia with Lewy bodies, and Parkinson’s? I’m having a difficult time understanding what the the differences are among these diseases. Are the amyloid plaques seen in Alzheimer’s similar to Lewy bodies, or completely different? Do stalls occur in Dementia with Lewy bodies, and Parkinson’s, or only in Alzheimer’s Disease? What is Frontal Lobe Dementia, and how does it differ from the other dementias mentioned above? Sometimes I see the word dementia capitalized, and sometimes I see it in lowercase. When should it be capitalized, and when should it be in lowercase?
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There are many terms here that are related. Dementia (usually with a lower case) is a general term that encompasses many causes of the symptom of decrease cognitive performance. The other terms describe different specific diseases which share some features. Several disease are associated with a buildup of proteins that can form deposits like plaques, but which protein is dominant differs. In Alzheimer’s, the deposits are mainly amyloid-beta, but most patients also have some tau accumulation. In frontotemporal dementia, tau accumulates. In Lewy body disease and Parkinson’s, alpha-synuclein accumulates. Everyone, even healthy, has a little bit of all of these proteins.
Interestingly, researchers recently have found that there appear to be stalls in the brains of mice that overproduce a type of tau protein. We don’t yet know whether these stalls have the same cause as in Alzheimer’s. It will need to be answered in a future study.
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Thank you for your reply. Lewy body disease, and Parkinson’s appear to have the same underlying cause yet they are considered to be two distinct diseases. Someone with Lewy body disease can have many of the symptoms associated with Parkinson’s, and yet not have the Parkinson’s diagnosis. What is the difference between these two conditions? Why are they considered to be separate diseases?
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Lewy body and Parkisons are similar and are likely related. They both involve the accumulation of the protein alpha-synuclein. The symptoms are slightly different which is one basis for defining these as different diseases, but it is still possible that both disease share an underlying cause related to the protein accumulation. I don’t think we known why the two diseases seem to share some aspects, but differ in the effects on a patient’s specific cognitive and motion symptoms.
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