Okay. Bear with me. I'm overloaded with information and I'm just beginning to understand and sort out what I've learnt. Piece by piece. Step by step.
Exactly what do the experts say it is?
Interestingly enough, they now are determining that it actually falls in the center of the spectrum between Alzheimer's Dementia (AD) and Parkinson's Dementia (PDD).
Wow! Say you! However can that be?
Well, after doing my own research, and reading many articles and watching several videos and webinars (many of which I will spare you, but they do have marvelous information!) I'm beginning to feel excited and stimulated about learning more and more and more! It's actually fascinating.
With Parkinson's Disease, and Huntington's, the lesions seem to predominate on this portion of the brain which leads to a loss of Dopamine to the Striatum portion of the brain. This is also called The Forebrain. This section of the brain is responsible for learning, motor control and a substantial number of other cognitive functions, which are then delivered to the ganglia for more processing.
(Whew!)
First of all, Dopamine is produced thoughout the brain. Dopamine serves as a neurotransmitter and is a precursor of other necessary materials used by the brain, such as epinephrine.
With Lewy Bodies, The inclusions (or Lewy Bodies) are more predominant among other areas of the brain, including the Cerebral Cortex, where most of the brain's functioning occurs. However, they are still present in the Striatum. This prevents the brain from delivering the Dopamine to the other relevant parts of the brain - but as I can see, it's not so much there as it is elsewhere. Here's where I have to tell you I'm fallible.
With Parkinson's, as the disease progresses, there is a greater and greater loss of Dopamine in the Striatum. And, the loss appears to be more asymmetrical.
With Lewy Bodies, the loss of Dopamine is similar to that of PD patients in the Striatum, but the loss is considerable compared to those with Alzheimer's, or AD.
Also, the loss of Dopamine in LBD patients in the Striatum is more symmetrical than that of PD patients.
The use of PET and SPECT imaging can reflect the differences in Dopamine loss between AD patients and LBD, but not between LBD and Parkinson's.
Now, AD patients also show a greater number of Corical Protein Beta-Amyloids, or Plaques, which are folded proteins on the brain, which in this case are abnormal, and cause the dementia, along with tangles of neurons.
Those with LBD showed these same Cortical Amyloids, but to a much lesser degree, while they are even fewer in those with PD.
Now, even with PD, having these cortical Amyloids creates motor and cognitive disfunction, so you can imagine that with AD and LBD these deposits would afflict greater harm.
Here is where I will cease for now. I will continue to build on this in the near future, as time allows.
UPDATE: Mother has her appointment scheduled for the Neurologist who is well into the LBD investigations on Tuesday, 6/10. Hopefully we will be well-armed with questions, concerns, and some semblance of knowledge!
At this point, Mom is confused, and bounces back and forth with her thoughts.
She latches on to a thing, such as her watch, and keeps coming back to it. The staff has also found she is obsessed with her hand cream that was prescribed to her.
Perhaps her latest agitation is because of another resident passing this past week, and it was someone Mother knew in the past, as well as someone her friend, Nancy knew as well.
We don't know. But we are realizing more and more that routine is vital!
I've been feeling rather ignorant, at sea, drifting in the wind, or what have you, about what the causes are of Lewy Body Dementia.
Exactly what do the experts say it is?
Interestingly enough, they now are determining that it actually falls in the center of the spectrum between Alzheimer's Dementia (AD) and Parkinson's Dementia (PDD).
Wow! Say you! However can that be?
Well, after doing my own research, and reading many articles and watching several videos and webinars (many of which I will spare you, but they do have marvelous information!) I'm beginning to feel excited and stimulated about learning more and more and more! It's actually fascinating.
Dr. Lewy
Lewy Bodies were first noted by Dr. Frederic Heinrich Lewy in 1912. He didn't notate, though, that the neruonal inclusions (Lewy Bodies) were typically included in the mid-brain structure called the Substantia Nigra, which controls voluntary movement, regulates mood, and produces the neurotransmitter, Dopamine.
Substania Nigra Diagram
(Whew!)
First of all, Dopamine is produced thoughout the brain. Dopamine serves as a neurotransmitter and is a precursor of other necessary materials used by the brain, such as epinephrine.
With Lewy Bodies, The inclusions (or Lewy Bodies) are more predominant among other areas of the brain, including the Cerebral Cortex, where most of the brain's functioning occurs. However, they are still present in the Striatum. This prevents the brain from delivering the Dopamine to the other relevant parts of the brain - but as I can see, it's not so much there as it is elsewhere. Here's where I have to tell you I'm fallible.
With Parkinson's, as the disease progresses, there is a greater and greater loss of Dopamine in the Striatum. And, the loss appears to be more asymmetrical.
With Lewy Bodies, the loss of Dopamine is similar to that of PD patients in the Striatum, but the loss is considerable compared to those with Alzheimer's, or AD.
Also, the loss of Dopamine in LBD patients in the Striatum is more symmetrical than that of PD patients.
The use of PET and SPECT imaging can reflect the differences in Dopamine loss between AD patients and LBD, but not between LBD and Parkinson's.
Now, AD patients also show a greater number of Corical Protein Beta-Amyloids, or Plaques, which are folded proteins on the brain, which in this case are abnormal, and cause the dementia, along with tangles of neurons.
Those with LBD showed these same Cortical Amyloids, but to a much lesser degree, while they are even fewer in those with PD.
Beta-Protein Plaques
Here is where I will cease for now. I will continue to build on this in the near future, as time allows.
UPDATE: Mother has her appointment scheduled for the Neurologist who is well into the LBD investigations on Tuesday, 6/10. Hopefully we will be well-armed with questions, concerns, and some semblance of knowledge!
At this point, Mom is confused, and bounces back and forth with her thoughts.
She latches on to a thing, such as her watch, and keeps coming back to it. The staff has also found she is obsessed with her hand cream that was prescribed to her.
Perhaps her latest agitation is because of another resident passing this past week, and it was someone Mother knew in the past, as well as someone her friend, Nancy knew as well.
We don't know. But we are realizing more and more that routine is vital!
- Also, please note that there were several sources used in today's blog, many of which I linked to for your continued education.
- I do owe thanks, as well, to LBDtv and SNMMI for their wonderful (but terrible sound) webinar on Molecular Imaging from 10/12/2012, with Dr. Martijn Muller.
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