How Are Alzheimer’s and Parkinson’s Diseases Diagnosed?

*The following is the output of transcribing from an audio recording. Although the transcription is largely accurate, in some cases it is incomplete or inaccurate due to inaudible passages or transcription errors.

The following podcast is provided by a Thera Farma and answers for elders radio and welcome back everyone to answers for elder’s radio network. On behalf of the theory of farmer and we are speaking again to one of the most amazing doctors, and I if you have been with us on our first segment. This man is very fascinating. I love listening to you and I’m learning something a lot so anyway. But we are with a Dr Michael Mega, and he is the director of the Senator Center for Cognitive Health in Portland, Oregon. and Dr Mega, you are amazing. So thank you so much for sharing your knowledge and and I love how simplist simple you made it for us to understand. So I want to talk a little bit in this segment about treatment. Let’s just say, for example, mom is diagnosed with Alzheimer’s. You know what happens at that point in and what is your standard? You know that you that you do, or Parkinson’s, etc. Okay, Susan. Well, that’s a great question, because the field is rapidly changing in Alzheimer’s Disease Treatment options. First off, I need to let your audience know that we now have biological markers for Alzheimer’s disease. In the past, we couldn’t make the definite diagnosis of Alzheimer’s Disease Prior to these biological markers emerging, until somebody passed away and we were able to look at their brain microscope, and then we could determine her certainty that Alzheimer’s pathology was present, in the sense that we were able to see then under the microscope, plaques that are made up of misfolded amyloid protein and angles that are made up of misfolded taw protein. In fact, misfolded proteins in the brains of individuals is the common thread for all degenerative diseases, including Parkinson’s disease, Loo Garrick’s disease, frontal temporal degeneration, picks disease, etc. So being able then to visualize plaque and tangle, now, through pet scans that are are given to people in life, we can make the definitive diagnosis of Alzheimer’s disease in people even before they start having memory problems. And may say we now know that plaque is deposited maximally in the brains of people who are on the Alzheimer trajectory about fifteen years before they start having memory issues. And it’s only the right is only when we start seeing the tangles form after plaque deposition, which actually kills the cells, that we start having symptoms emerge. And so plaque is deposited first, then a cascade of pathology kicks into gear, the misfolding of Taw which forms the tangles inside the cell and then kills the cell. Furthermore, not only do we have pet scans that visualize these plaque and tangle depositions in life, there are also now blood tests being developed that can measure the amount of tangles in the brain that leak out into the cerebral spinal fluid and then eventually into the blood, so that blood tests are now being developed for identifying people who are on the Alzheimer trajectory. So that’s a huge thing. Furthermore, many types of treatments are being developed to stop the missfolding and deposition of plaque in the brain, as well as the misfolding and deposition of tangles in the brain, and so it’s hoped that we have for the future a blood test that people will go to get at their primary care doctor’s office when they go for their yearly health, healthy yearly physical, that would identify whether or not they’re on the Alzheimer trajectory and then institute disease modifying drugs to keep them from getting Alzheimer’s disease if they haven’t already developed memory problems. That’s amazing. At is amazing. You know, this could totally change, you know, the whole picture of Alzheimer’s disease because so many, you know, I know in Washington state. I don’t know how it is where you live in Oregon, but I know we’re one of the highest per capita here in our state of Alzheimer’s disease. Yeah, so it’s kind of interesting and and to look at. You know, how many people are caring for those with Alzheimer’s. It’s the statistics are overwhelming and certainly for families that are going through this devastation with their loved one. You know what an amazing thing you can do to catch it early before manifests itself. That is incredible. That is that is the goal. Here in Portland, however, we don’t have quite as high because this is a city where young people come to retire. So we have more young people perhaps and thus less of a risk. Ye, how well you know? I guess there’s a lot of differences. I guess I’ve heard in Washington state something like I think it’s close to hundred and fifty thou of our citizens in the state of Washington have are afflicted with Alzheimer’s disease and they’re being cared for by over three Hundredzero family care partners or caregivers. So it’s it’s a big deal in the state. And so obviously the is the disease affects more than just the person with it at the ranks the whole family. It certainly does. So obviously we’re talking about Alzheimer’s disease. Let’s switch over to Parkinson’s. How if someone is somebody is diagnosed with Parkinson’s, what would be the you know, the trajectory, our path on tweeting that. So, as you had said earlier in the previous podcast, there is a related disease called Louis Body disease, and so the distinction between Louis Body Disease and Parkinson’s disease is somewhat moot. In fact, if when we look at the brains of individuals who have Louis bodied disease versus Parkinson’s disease. They they look the same in terms of the deposition of another misfolded protein called Elpha Sin Nucleon that makes up a Louis Body. And Parkinson’s patients have Louis bodies deposited in their brain, and so do Louis Body disease patients. It’s right the location of where these Louis bodies are deposited that produce distinctly different clinical manifestations. So if Louis bodies are primarily deposited in the brain stem or subcortical structures and produce damage to those subcortical structures, those tend to manifest first as slowness in moving, as well as tremor gait and balance difficulty. Right versus if they’re primarily deposited in cortical structures as well as brainstem structures, that produces more of a cognitive problem, with problem solving difficulty, visual spatial issues, hallucinations, as well as fluctuations and attention. Yeah, and many Louie body patients end up having some movement problems manifest after their thinking problems manifest, and so, in fact that’s part of the diagnostic criteria in Louie body disease that movement abnormalities tend to happen after the cognitive abnormalities, and so we would make the diagnosis of Louis Body Dementia clinically if somebody had three of the following things around Behavioral Sleep Disturbance, where you act out your dreams during your sleep, visual hallucinations while you’re awake, and they can be little animals or cartoon face stare share fluctuations in attention or alertness, as well as what’s called neuroleptic sensitivity, which many people who have hallucinations are given neuroleptic drugs that are antipsychotic drugs by their physician, and some of these older generation neuroleptic or antipsychotic drugs can produce a locked in syndrome that shows a very strong sensitivity to those drugs, and thus it’s called neuroleptic sensitivity. And so if somebody has three of those four things, they are said to have Louis bodied dementia. If they’re family members say they are no longer safe to live alone. Remember, that’s the definition of dementia. No longer being safe with independent living now. That’s different from Parkinson’s disease, who only fifty percent to Parkinson’s patients will develop a thinking problem where their families say they are no longer safe to live by themselves, thus having dementia only fifty percent. Most Parkinson’s patients don’t have significant thinking problems in the very beginning of the disease when they have more tremor gait problems or difficulty initiating motor movements. Right. So you can see that the clinical distinction between these two diseases is rather stark, even though the pathology in the end is due to the same misfolded protein Elphasin NUCLEU. Yeah, and it’s so interesting because I have known of stories of guests that have been on our shelf and they tell the story of those with Parkinson’s. Sometimes music, like in the gate, you were talking about gate, that there’s an ability like where all of a sudden you start to sing a song and it’s like they’re they’re able to pick up the gate or whatever it is. So it’s kind of fascinating. How yet it doesn’t necessarily equate to specifically dementia, but it has to do with a motor skill and did I express that correctly, doctor? Yes, yes, that’s good. Also, the common treatment for Parkinson’s disease, Carba Dopeleve Adopo or Cinemat, has very good efficacy in helping the slowed movement, what we call Brady Knesia, and sometimes the slow thinking what we call Brady Frennya. And so people who have purely Parkinson’s disease get really good effect from Cinemat, whereas people who have Louis Body disease, when they develop the motor abnormalities that look Parkinsonian in right slowness and in movement, tend not to have as robust a response to Cinemat as the pure Parkinson’s patient. And so clearly there’s also a difference in response in terms of the typical treatments that are given to people with Louis Body disease versus Parkinson’s disease. Well, and Dr Mega, I want to talk about in our next segment a little bit about the trial, what our goals are for the trial, what and you obviously are working with patients right now and are seeing some results on the trial. And so, first of all, for those of you that want to watch our next are listen to or watch on youtube our next segment. Certainly go to the website www dot ad trialcom. That’s L I ft a D like stands for Alzheimer’s Disease Trialcom, and make sure you can do that. Or you can just go to shape, shape trial trialcom. Either way you learn a little bit more about the program that is we’re about to talk about in our next segment with Dr Mega, and we’ll be right back right after this. The preceding podcast was provided by a the reformer and answers for elders radio. For more information about the Alzheimer’s clinical trial, go to a thera clinical trialscom.