Wednesday, July 2, 2014

The Differences Between AD, LBD and PDD - Part II - in a nutshell

So, last month, I spoke of the Amyloids, plaques, and the Lewy Bodies in their parts of the brain, which helps tell what form of dementia the afflicted has.

Now, do understand, as well, that the best diagnosis made is one that is "Probable".  They cannot diagnose definitively until autopsy, as the neurologist stated.  This is understood.  And, with the high cost of the SPECT, PET, and other imaging processes, this is just not doable unless, of course, Mother and her peers who suffer from the affliction, had a great deal of money (a lottery winner might have enough).  So, we do what we can.

Now, back to the plaques which affect parts of the brain.  According to the NIH, plaques are a normal part of the aging process.  They still aren't completely sure how they work, but they do know that people with AD seem to have quite a few.

The plaques come down and live outside the membrane of the brain cell.  They normally would be fought off (from my understanding of the literature), but with AD and dementia, they seem to cleave in and take hold, never quite letting go.  This is due to the enzymes which are involved.
from www.nia.nih.gov (Alzheimer's Disease: Unraveling the Mystery)

One form of enzyme that takes hold is benign.  With AD, the enzymes are not.  In fact, they begin to clump together and resist the cells "fighters" to send them thither and yon.  Once they take hold, there are others that come down and clump with them;  the proteins that make up a goodly part of these are misfolded, and are not benign.

                                        from www.nia.nih.gov (Alzheimer's Disease: Unraveling the Mystery)

There are also the Tangles.  These tangles are made up of the Tau Protein, which is inside the cell.  Normally, there are a certain number of these Tau Proteins which are attached to microtubles.  On these Tau's, there are attached a certain number of Phosphate Molecules, and thus the cell is able to function.  With AD, though, there are a more unseemly number of the Phosphate Molecules that attach themselves, and tangle the strands of Tau and the microtubles, which lead to the cell's death from the inside.

And then, with AD, there is the death of the cell, and the loss of communication between the cells. This comes, as I understand, from the above reasons.
For more about this, I suggest you visit:  Alzheimer's Disease:  Unraveling the Mystery.  This is  a very interesting, but technical insight into the causes of the disease.
                                                                    loss of connectivity between cells 
                                              from www.nia.nih.gov (Alzheimer's Disease: Unraveling the Mystery)

What has this to do with Lewy Body? Well, as I mentioned in the earlier blog (Part One), on a scale, from which Alzheimer's Dementia (AD) is on one end of the specturm, and Parkinson's Disease Dementia (PDD) is at the other, Lewy Body Dementia (LBD) is somewhere in the middle - thereby demonstrating symptoms that have elements of both AD and PDD, as well as some Parkinsonian Disease, in tremors, movement, etc.   So, it wouldn't be wrong to state that Mother possibly has some of these plaques and tangles killing off cells and neurons in her brain (nor would it be wrong to state this happens in other elderly people, either, as it is somewhat common, but not as rapid-paced as it is with those afflicted with either of the two dementias).

Now, interestingly, the Amyloid-Plaques are very vivid on the molecular imaging with LBD, as well as with AD.   Interesting, isn't it?!

Now, with PDD and LBD, though, the cortical amyloid plaques affecting cognition and movement can be detected and monitored (remember it's expensive - so if you're not part of a study, you'd better have saved) using some experimental treatements  (Discover MI.org.  2012).

Let's move on now, to Acetylcholine.
  1. a compound that occurs throughout the nervous system, in which it functions as a neurotransmitter.

 This is a neurotransmitter which is shown to diminish with more extensive and rapidity  with PD and LBD, to a somewhat different extent than with AD.  Why?  I'm not quite understanding it myself.   But the acetylcholine loss is in the 15-30% range on average for both these dementias. These dysfunctions appear at the same rate early on, which accounts for Mom's problems in the recent past, and her needing to be where she is.

In the next addition to this portion of the blog (Part III), I will write more on the Cholinergic loss, and it's detriment to balance and movement.

Here, I would like to bring out some resources that are very informative:

A webinar on Molecular Imaging and the Spectrum of AD, LBD, and PDD

The National Institute on Aging:  Resources for Lewy Body Dementia.  Here you will find an online copy of the book about LBD, which Jean, Mom's buddy, ordered several copies and passed them out to those who have an interest in the disease.  For those of my family, I have a few copies, as well, and if you ask, I will hand them to you - otherwise, you may call and request free copies for yourselves and others.

The Lewy Body Dementia Association has a marvelous site with all sorts of information and news.

There is also the Alzheimer's Reading Room, which is run by a guy named Bob DeMarco.  He brings in several interesting articles about dementia.  He began when his mother was diagnosed with AD, and he has continued writing on all sorts of interesting items while he cares for her (she's 93).  It's truly awe-inspiring when you realize just how much effort and work he's put into his work.  There's even a search bar which is very helpful!


There are many other sites.  I do, myself, have the Lewy Body Dementia Support/Blog Page on Google+, on which I post, and so does Mr. DeMarco, and others.  I am hoping to have many others join us, as well.






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