7.27 interview log plus notes.docx

85:

 

0.00: Non-molecular, people’s perspectives.

Different people different perspective. Starts with memory problems, then other cognative problems. Gets worse, leads to social withdrawal. There are people who start with different pathways: emotional problems very early on : thought to be starting at the frontal lobe. Incidence of a women with hallucinations, etc.

Sometimes easy to tell that patient has alzheimer’s disease, when symptoms are beyond that associated with age; sometimes very difficult. Happens a lot. Especially with younger people. Emotional disruptions: agitation, anger, hallucinations, delusions, etc. Is a varied disease.

4:00 how they diagnose it? Tests?

Most common symptom: memory loss.  Hard to find words. Lost driving. Ask: do you rely on organizational methods more; is there a change in their memory abilities? Once in a while, memory is not primary problem: sometimes language problems. There is a set primary progressive problems called “primary progressive aphasia” (Primary progressive aphasia (PPA) is a form of cognitive impairment that involves a progressive loss of language function.) Certain subsets of these language problems from people with alzheimer’s disease. Initial presentation of Alzheimer’s can be anything (language, visual, special, executive).

7:15 sometimes easy, sometimes hard. Sometimes masked, especially in smart/bright people. 80yo MIT civil engineer: had memory problems, yet sometimes in discussions in his office, he was brilliant. So, very difficult to tell with that presentation. Also, very hard to tell someone that they have Alzheimer’s: when you’re not sure, you don’t want to believe, at least this doctor doesn’t. But you have to be objective. You take a history of all the problems, you do examination: little tests – attention, language (naming, talking pattern problems, forget what they meant to say), (digression: remembering structure of sentence same as remembering what you ate for breakfast? Probably not. Blah, blah that’s his area of interest.) Alzheimer’s patients often have the problem of forgetting what they said, repeating, getting lost, asking for questions to be repeated. So, tests to test memory: asking to repeat words immediately, after 30 secs, hiding things around the room (visual memory).

15:00 more tests. Test skilled actions (these can be affected too) Eg, pantomiming actions. Can write in block letters, but not in cursive. (bad audio at this point). Cannot test everything, so they will miss something. Not good at testing control systems (eg, note taking: what to write down and what to leave out relative to your goal for doing the interview), but they try. Interesting explanation as to why saying the names of as many animals as you can in a minute is a test of control (executive functions) rather than memory or language.

20:00 The goal is see if person is performing as expected given age, education, etc. Doctor person said, “all of this is subjective”, but there is sometimes no question in a trained professional’s mind that the person has alzheimer’s. Times when you are pretty sure that the person is normal, but then times you just can’t tell. (Jesus Christ, police siren in the background). Then you send to Neuropsychologist, who tests their abilities against control groups. Also, you look for things that are missing, eg, parkinsonian tremors, etc., because other diseases can also affect memory and you have to think twice about Alzheimer’s. So, do tests that look at metabolic functions, renal functions, etc. to check for diseases that could be affecting memory.

22:30 Do brain scans to see patterns of atrophy associated with AD. AD starts at the hippocampus in most cases, so check out the hippocampus (note, if there is to be atrophy in the brain, then there disease must have progressed very far!). Look at family history. People don’t routinely do genetic tests for Alzheimer’s but there are people who routinely do genetic tests for patients under 60, for APOe, Presenilin, etc.

25:00 is it possible to do early detection? This is where the field is at now. There are people working on it, stop processes before they are advanced. (25:40) There are 3 other tests. FDG pet scanning, hypo metabolism, parietal, temporal lobes. Imaging for AB : using compound called flow-betapere(?) (improved version of pittsberg compound). Ratios of AB, tau, phosphoralated tau in Cerebrospinal fluid (requires puncturing the vertebral column.) But you can’t do lumbar puncture in everyone you think has alzheimer’s—large number of people.

27:30 what can you do about it if you detect early? Very little. Keep healthy. Intellectually, socially, engaged.  Nothing we can do about AB or tau, but if you are healthy, you will do better. You’ll live a good life, and you’ll be able to fight depression

32:00 two drugs that directly fight AD. Statistically, they don’t improve function, but delays degradation. Gives you two-three years of cognitive function extra. But that is not what we are looking for. Not even as good as drugs for parkinson’s. Lots of clinical trials to affect biology.

 

86:

0:00 a story about doctors are being asked questions that are not medical questions. Then talking about people coming in and showing classic alzheimer’s symptoms, but about him being wrong about so many of them, giving him extra respect for lab tests, prolonged observation, etc.

3:00 patient experiences. Differs from people to people. A lot of people have trouble grasping the idea and transitioning. Story of difficult coping for a military man. Taxing on caregivers. (8:00)

9:00 good things about Alzheimer’s Society.

10:00 life expectancy. (Not the expert on it)

12:30 “big burden of care”.

Ends with his personal experience with AD.

 

 

 

Couple of points:

Int 1: talks a lot about the  psychological tests for AD. There are genetic tests for common proteins in younger patients, but not routine. Some “chemical” tests/scans available for detection, but problems with that (look up). But there is nothing we can do to prevent it even if we know early on, right now.

Int 2: Thinks that if AD is detected early, then many of the drugs that failed in the later stage can work if administer early enough. About delivery, thinks delivery is a field on its own. So, if treatment works, then is the delivery will follow. (but we should make a point that we kept the delivery in mind while designing the treatment).

 

Int 1: should look at the 3 types of (non-psychological) tests he mentioned. Why are they not widely used? “(25:40) There are 3 other tests. FDG pet scanning, hypo metabolism, parietal, temporal lobes. Imaging for AB : using compound called flow-betapere(?) (improved version of pittsberg compound). Ratios of AB, tau, phosphoralated tau in Cerebrospinal fluid (requires puncturing the vertebral column.) But you can’t do lumbar puncture in everyone you think has alzheimer’s—large number of people.“

 

 

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