‘Don’t Let Doctors Dismiss Your Concerns:’ A Neurologist on Diagnosing Dementia

By | September 27th, 2023

Neurologist, author, and Alzheimer’s expert Marwan Sabbagh discusses why dementias are so difficult to diagnose accurately — and what patients should do if they think they may be experiencing symptoms of cognitive decline.

Getting an accurate diagnosis for a neurodegenerative disease like Alzheimer’s or another form of dementia early in the journey can make a huge difference for patients and their loved ones. An early diagnosis means more time for cutting-edge treatments, lifestyle changes, spending more time with loved ones, and even joining clinical trials. On the flip side, a misdiagnosis could mean that patients receive the wrong medications or have serious negative health outcomes in the long run. In our Patient Perspectives series, we’ve seen firsthand how long getting the right diagnosis can take. 

So, why is misdiagnosis so common, and what can doctors, patients, and caregivers do about it?

To answer that question, we asked neurologist, author, and Alzheimer’s expert Dr. Marwan Sabbagh on Live Talks to discuss why dementias are so difficult to diagnose. Sabbagh, a board-certified behavioral neurologist at Barrow Neurological Institute’s Alzheimer’s and Memory Disorders Program and a professor at the institute’s Department of Neurology, has served as the lead investigator on a number of prominent national Alzheimer’s prevention and treatment clinical trials. In this talk, he’ll speak to the factors that make dementia so difficult to diagnose accurately for experts and clinicians — as well as what patients and their families can do to advocate for an accurate diagnosis and a faster response to brain health concerns.

Read or watch his full conversation with Being Patient EIC Deborah Kan below.

Being Patient: Why is it so hard to diagnose people with Alzheimer’s disease?

Marwan Sabbagh: This has been kind of the bane of a lot of industries’ existence is that they’re afraid that there are all these new drugs, exciting developments, and nobody can diagnose it. Fundamentally, it boils down to the fact that primary care physicians don’t feel comfortable making a diagnosis. They get 36 months of training, one month of neurology; if they’re lucky, they get one day in the cognitive clinic. Yet we lay everything on the back of a primary care physician who does not feel comfortable making these diagnoses, and the consequence is that they delay the diagnosis. They delay referring, they don’t feel like it’s necessary to screen patients. They dismiss symptoms, “Oh, you’re depressed, you’re tired, you’re sad, you’re this or that”, but they don’t take it head on, and that’s been a problem.

Being Patient: Most people I’ve spoken to who I know have gotten a diagnosis. It always starts with MCI. Tell us a little bit about diagnosing MCI.

Sabbagh: Both MCI and dementia are categorical definitions, Deborah. That means that MCI is cognitive impairment without functional impairment, still independent, but still having some cognitive issues. Dementia is a category of definition of cognitive impairment with functional impairment. We want to capture people in the MCI phase. I think doctors don’t know when a person goes from MCI to dementia. Even in the lay audience, [people don’t] understand that Alzheimer’s is a type of dementia. So, [dementia is the] category, Alzheimer’s [is the] type. Physicians themselves mix these terms up. But I think that they use the term mild cognitive impairment because they notice something wrong, and they don’t want to use the boogeyman word of dementia, so they say it’s mild cognitive impairment. 

“We want to capture people in the MCI phase.
I think doctors don’t know when a person
goes from MCI to dementia.”

I have to tell you, though, what physicians have learned. This is the other problem we face, Deborah, is that we learned in medical school that you can only diagnose Alzheimer’s with an autopsy. That is still taught to this day in medical school curriculum, even though you and I spend our day jobs seeing the newest biomarkers, the newest breakthroughs, and the newest tests; doctors think you can only diagnose Alzheimer’s in an autopsy, that you can, you know, you just check a B12, TSH and an MRI and by default, you have a dementia diagnosis, and you know, and I know that’s just not accurate.

Being Patient: I think at that early stage, it’s hard to give someone a cognitive assessment unless you know what their baseline was right before they were expected to have memory loss. I even tried this on my own mom when she was first diagnosed. I think I gave her a MOCA test every day for three weeks, and it was vastly different according to what her mood and her state were that day. Do those cognitive assessments actually give us an accurate assessment?

Sabbagh: I actually feel like that’s one of the problems and challenges we face as practitioners, and we kind of bank heavily on what the cognitive test is. I have proposed and published on the idea that we should first do informative-based questionnaires, and there are many of them now. That’s to say, a physician’s asking an informant information about cognitive issues. There’s the AQ Alzheimer’s questionnaire, the ADA IQ quote, now called the EQRS. These are ways for the physician to capture if there’s incident cognitive decline. As an added value, I do that before the cognitive assessment.

Being Patient: What types of questions are being asked on these informative-based questionnaires?

Sabbagh: The Alzheimer’s questionnaire is not to the patient but to the informant: Is there a memory issue? How long has it been going on? Do they forget appointments? Do they misplace objects? Do they get lost, become disoriented, and have trouble handling money? 

I actually published a lot on the Alzheimer’s questionnaire, and we use it in our practice. I’ve been using it for years on hundreds of patients, and correlates very well with a lot of other instruments as well. That’s the instrument we use in Arizona, but there are a lot of other instruments. AD8 is the most common, Alzheimer’s disease eight, that’s Jim Gallons IQ codes, and then a new one called the EQRS.

Being Patient: After you have that first line of questioning, would you then do a cognitive assessment, or what’s next?

Sabbagh: I would do cognitive assessment. The most common, of course, is the MOCA, but the Mini-Mental, the SLUMS, the Mini-Cog, whatever you’re comfortable with. I actually love Kivipelto’s. Not everybody knows her for the Finger study; before she ever did this Finger study, she did something called the CAIDE score, and it’s basically a risk score of Alzheimer’s.  I actually embedded that in my practice. So if their CAIDE score is high, and their AQ is high, and their functional assessments, stage, and skills high, I know I’m dealing with something in the mild cognitive impairment or dementia, degenerative in nature. I also do a Lewy Body screening questionnaire. What I’m saying is, by the time I get to the physical neurological exam, I can tell if they’re normal, mild cognitive impairment, dementia, and I’m just checking the boxes at that point. So use the HPI, history of present illness, and all the questionnaires to drive what I’m doing in my evaluation.

Being Patient: Before we get on to different dementia, I want to talk a little bit about the diagnosis from MCI to Alzheimer’s disease. How do we know when MCI is Alzheimer’s disease? How do you diagnose that?

Sabbagh: These are the terms that people kind of mix and match. The fact is that MCI, as a categorical definition, means, like I said, cognitive impairment without functional impairment. MCI only is a descriptive term, and the charge is to figure out what is the cause of MCI. I will call people mild cognitive impairment due to Alzheimer’s disease if I have the CSF or the PET or something else, and then  Lewy body or Parkinson’s or Frontotemporal dementia, so you always say MCI due to “dot dot dot” dementia due to “dot dot dot.”

“MCI only is a descriptive term, and
the charge is to figure out what
is the cause of MCI”

I always start with the categorical definition and the aetiological definition. So, people will say, “Whew, I don’t have Alzheimer’s,” I’m like, “Well, you have MCI, and you’re showing biologically changes that will lead to dementia and Alzheimer’s dementia in particular.” I spend a lot of time explaining that.

Being Patient: Let’s talk a little bit about those changes, too, because now we have blood tests to detect beta-amyloid plaque. Usually, though, that’s only available to people in trials. It’s not usually presented to the patient yet. Could it be coming?

Sabbagh: I actually started ordering them last week in the clinic.

Being Patient: I am assuming right now, you’re rare?

Sabbagh: Yeah, I’m very rare. We’re on the front end of everything, so we get to do it all before everybody else does. That’s what’s cool about my job.

Being Patient: With blood tests not fully accessible and PET scans being hugely expensive, how does a doctor determine whether or not there’s plaque or tau? Are there options other than a PET scan or a spinal tap?

Sabbagh: I do the spinal tap, and I recommend it, and PET scans, you’re right, are still out of reach. For most people, we’re running about one a month when patients are willing to pay out of pocket until there’s a rumor in our world, as you know, that Medicare might change their mind in the very near future, although that has not materialized yet [as of October 2023, beta-amyloid PET scans are covered by Medicare]. 

The bottom line is I tell them to make the determination as to whether this is Alzheimer’s, or if it’s going to get worse, we need to do the lumbar puncture or the spinal tap, and they’re all gonna cringe. But the fact is, it’s about how we present it. I will tell you, we do lumbar punctures for meningitis, encephalitis, multiple sclerosis, and a dozen, two dozen other things, and there’s no reason not to do them for Alzheimer’s. I do them in my office. We do [it] in the radiology department. It’s not a scary thing like it used to be perceived. It’s a five-minute office procedure, and I tell them that we’re doing it a couple of weeks in our office, and it’s going fine, I do it myself.

“ I will tell you, we do lumbar punctures for
meningitis, encephalitis, multiple sclerosis, and
a dozen, two dozen other things, and there’s
no reason not to do them for Alzheimer’s”

Being Patient: The reaction that I hear from patients about a lumbar puncture is that it hurts, or sometimes it’s hard to find the areas that it’s really narrow. I think that’s why it seems scarier than a scan.

Sabbagh: I’ll tell you if there are a lot of reasons not to not do it in the office will send it to the radiology department, where they do it under fluoroscopy. But, a lot of times, I do it myself if there. It’s also experienced, I mean, there are actual practices that have dedicated practitioners that just spend their time doing spinal tap. It’s not as big a deal as people make it out to be. This is the time that the popular impressions and the science are a little bit incongruous. 

Being Patient: Are spinal taps much less expensive and covered by insurance?

Sabbagh: They’re covered by insurance. All told, all costs, including the procedure and the analysis, are about one-fourth of what a PET scan costs. They are covered nowadays. We need to get the authorizations for the analysis, not for the lumbar puncture. The lumbar puncture is a standard neurological test covered every single day in the clinic, it’s the analysis you have to get approved.

Being Patient: Can you detect both beta-amyloid and tau in a spinal tap?

Sabbagh: Both! [We can look at] two forms of tau and one beta-amyloid, so we actually look at it all. 

Being Patient: Is it true that you need plaque in order to have a diagnosis of Alzheimer’s?

Sabbagh: Correct. You can have another neurodegenerative disease without amyloid or without plaque, but that’s not Alzheimer’s. It’s something else. In order to have Alzheimer’s, you must have amyloid plaques in the brain.

“In order to have Alzheimer’s, you must
have amyloid plaques in the brain.”

Being Patient: I think the confusion arises because there are people who have plaque in their brains and never see a symptom of Alzheimer’s. They have the hallmarks, but the symptoms of the disease aren’t present.

Sabbagh: A lot of people say, “Well, the amyloid is not sufficient.” That’s partly true. What we know is that there is an inflection point where amyloid starts to cause damage, and that damage is through the tau and tangles and the spread of tau and tangles. So, amyloid does not correlate well with clinical symptoms, as you know, but tau and tangles correlate very, very well with clinical symptoms. It’s the spread of tau and tangles that correlates with clinical symptoms, but the event that leads to the creation and formation of tau and tangles is the presence of amyloid,

Being Patient: In other words, people can have amyloid in their brain and not see a symptom of the disease, but usually, when there’s tau present, you’re experiencing symptoms,

Sabbagh: Correct. When they looked at all those people who had heads full of amyloid but never got dementia, it turns out it wasn’t the typical 42 amino acid, it was the 40. It’s what’s called the non-senile plaque. In other words, their amyloid is a little different. It’s not the stuff that leads to Alzheimer’s disease.

Being Patient: It’s not the bad amyloid. Now, I’m going to throw a few common scenarios at you that we hear all the time. The one that makes me most angry is a woman in her 50s or early 60s, she goes to her doctor, and she’s experiencing something wrong and out of character. If they’re that age, they’re told it’s menopause. We have people like Michelle Hall in our community, who is a lawyer and raises three kids, and all of a sudden she’s losing words, and she’s staring at words that she can’t spell anymore, and doctors tell her it’s menopause. How is it possible that a totally competent woman who raises three kids and has a full-blown career suddenly can’t speak and can’t recognize words? And, then, she’s being told it’s menopause?

Sabbagh: Several things to say there, Deborah. First, I just saw that a very important VIP, a board member of ours, actually, and in her early 50s [had the] same complaint. It turned out her pregnenolone was super duper low, and we gave her pregnenolone because we do have a comprehensive lab panel that we run on our patients,

Being Patient: What is pregnenolone?

Sabbagh: It’s a prehormone that becomes something that helps the brain work better. In fact, Robbie Brinton at the University of Arizona, she’s actually doing a clinical trial of allopregnanolone to treat Alzheimer’s. The reason I’m saying this is we repleted her pregnenolone, and her memory fog got much, much better. So why

Being Patient: Is that a supplement she was able to take?

Sabbagh: That’s a supplement, but it’s a prehormone. Actually, that’s a tangent. My point is that menopause can cause brain fog. I’m not going to deny that, but that’s not always the only issue. That’s the time I have started ordering the blood tests because at least then I can say, well, it’s not Alzheimer’s, right? Your plasma tau is normal, and your neurofilament light is normal; therefore, it’s not Alzheimer’s— let’s keep looking. Then we do the neuro psych testing, we check their sleep, we check their meds if you know what I’m saying. People are also self-medicating with stuff that makes their memory worse. Then we check for COVID, and we check for other things. I don’t automatically go to menopause, but a lot of people do.

Being Patient: For doctors who don’t have the resources that you have, should they be giving women a hormone test, and is there a certain level of maybe the drop in estrogen that would indicate that perhaps you have more brain fog?

Sabbagh: I know you have experts that can probably comment on that better than I do, but I will tell you, I have this comprehensive lab panel that draws a lot of things. homocysteine, thyroid, pregnenolone, and a lot of other things. What I’m saying is that I use that as a kind of guidebook to start to target things to optimize their health. Because everybody who has a memory issue is not always Alzheimer’s, right? 

I know you can have a memory issue that has nothing to do with Alzheimer’s. I see, still to this day, patients taking medicines that make their memory worse. I see patients who have severe problems with their sleep. I see patients with mood issues. There are a lot of things you’ve got to look at in a perimenopausal woman, and yes, on it is the chain, the delta in their estrogen that may have adverse effects on their cognition, but it’s not just that, and I will look at a lot of things.

Being Patient: What are some of the medications that you are aware of that impact memory?

Sabbagh: All cyclic antidepressants: amitriptyline, nortriptyline, imipramine. That’s number one. Number two is a lot of bladder medications: ditropan, oxybutynin also causes [memory loss]. A lot of meds. A lot of over-the-counter sleep aids: the Benadryl, the Tylenol PMs, anything that is an anticholinergic, anything that blocks cholinergic activity. So, the brain chemical response for memories is acetylcholine, there are a lot of drugs that actually reduce acetylcholine, and a lot of the antihistamines, anti-allergy meds that are the PMs of the world, Tylenol PM, not the Tylenol, but the PM. That’s the stuff that actually makes your memory worse.

Being Patient: Interesting, because I bet there are tons of people on those meds, right?

Sabbagh: In fact, before I ever see a patient, before I walk in the door to see a patient, the first thing I look at is their medication list. I am stunned to this day how often people are on meds that make their memory worse. You know, muscle relaxants, narcotics, benzodiazepine sleep aids, it just takes your breath away.

“There are a lot of reasons to have
memory issues that are not Alzheimer’s.”

I see a lot of patients who, if I just took away three-quarters of their meds, their cognition would clear up. If I fix their sleep, their cognition would clear up. There are a lot of reasons to have memory issues that are not Alzheimer’s.

Being Patient: I had no idea that so many of those medications interfere. I want to turn to different dementias because we have so many people asking questions about them. I believe, not as a scientist, but from my very unscientific poll of talking to people, that Lewy Body dementia is the most misdiagnosed dementia out there. I think there are actually more people out there with Lewy Body who don’t know it then there are other dementias—do you agree with me or not?

Sabbagh: I 100 percent agree with you. It is the second most common type of dementia, and nobody’s ever heard of it until Robin Williams had it. Then the list goes on, Casey Kasem— he died of Lewy body dementia. Ted Turner has Lewy body dementia. That’s a very common condition that nobody’s ever heard of, and so they look at me like, “What’s that?” I completely agree with you that it’s underdiagnosed, misdiagnosed, and often missed.

Being Patient: I want to tell you about Don Kent, a member of our community. When I interviewed him, he told me that he went to seven neurologists before he got a diagnosis of Lewy Body. Mayo finally diagnosed him because when he was eating, what was sweet tasted salty, and what was salty tasted sweet. They were like, “That’s a hallucination. You have Lewy body dementia.” It wasn’t that simple.  So, how do you diagnose someone with Lewy body dementia? What question should people be asking their doctor to get a better diagnosis?

Sabbagh: The core criteria are Parkinson’s change, motor changed Parkinson motor change, and cognitive, coming close together, meaning within a year or two of each other hallucinations, where they see things that are not there, fluctuations, meaning they’re better, worse, better, worse, better, worse, and then the last thing is acting out dreams. You know Jim Galvin very well. He’s probably been a guest on your program. Jim Galvin is at the University of Miami, he created a screening questionnaire called the Lewy Body Clinical Rating Scale. I actually use it in my medical practice every day, every time I see a patient, and it’s a great screening tool for Lewy Body dementia. If they score above six, there’s a high probability it’s Lewy Body, and if it’s below three, there’s a low probability of Lewy Body dementia, and I actually use it so much I embedded it in my electronic medical record. I can tell you the score of every single patient I’ve seen. If that scores high already, I’m driving down that road. I’m looking for all those core criteria.

Being Patient: Are there different types of Lewy Body that are more closely related to Parkinson’s?

Sabbagh: The real-world experts are the people in Newcastle and other places in the UK, Ian McKeith and his colleagues. The reason I tell you that is they believe there’s a psychotic variant, and then there’s a motor variant, meaning that there are people who have a lot of hallucinations, and other people have mostly motor and Parkinson’s changes. I’m not sophisticated enough to differentiate it, I’m not going with the sub-variants, I’m saying it’s Lewy Body.

Being Patient: Can you tell us what are some of the questions that are on that rating scale? How do you determine if it’s Lewy Body or another type of dementia?

Sabbagh: I will tell you a self-report of a memory complaint, I would lean toward Alzheimer’s, mainly because people are not self-reporting acting out dreams. They’re not self-reporting, whether they’re hallucinating or not. So, I would have to see other complaints from self-report to make that determination, I would also have to look at their clock draw. You were talking about the MOCA. I’m sure your mom aced this, the drawing of the clock.

Being Patient: Actually, the clock was the hardest part. I think the clock is the best diagnostic of the MOCA.

Sabbagh: A lot of people agree with you on that. There’s a company in Boston called Linus Health— they have done a digital clock draw. They believe the same thing as you do that the clock draw is an extraordinarily accurate test. If they’re very mildly affected, but they’re having trouble drawing a clock, I start to think about Lewy Body, certainly.

Being Patient: Wouldn’t the clock draw be as difficult for someone with Alzheimer’s?

Sabbagh: Not necessarily. [You could be] not as egregiously impaired.

Being Patient: That’s interesting because I think the translation of multiple layers of information with the clock is what makes it difficult because, with Alzheimer’s, you start to lose your ability to multitask, right?

Sabbagh: It has both organizational and visual spatial, so yes, the multitasking.

Being Patient: If someone is going to a GP and not speaking to a neurologist like yourself, what are some of the questions they should be asking?

Sabbagh: The patient should be asking about the new blood tests, the new scans, the new technologies; they should not be letting doctors dismiss their complaints. That makes me crazy. I have to tell you, when a doctor says, “Don’t worry about it, you’re depressed, you’re sad, you’re this, you’re that.” No, if the patient complains about their memory, they should evaluate it or refer on. That’s the one thing I would tell you is tell the patients to keep going and don’t let the doctor talk them out of it.

“The patient should be asking about the
new blood tests, the new scans, the new technologies;
they should not be letting doctors
dismiss their complaints.”

Being Patient: We got a question a while ago about somebody who had really bad alcoholism and was exhibiting signs of dementia. Is alcohol dementia a disease, and is it reversible, or does it set you on the track? What’s the relationship there with alcohol abuse and dementia?

Sabbagh: Absolutely. Chronic severe alcohol abuse causes three subtypes of dementia. If you want to get technical, it’s Wernicke-Korsakoff syndrome, Marchiafava-Bignami disease, and the alcoholic dementia Maurice Victor, but the point is that alcohol at high doses can cause severe damage and can cause dementia, usually knocked progressive. In other words, if they stopped drinking, they may not get worse, but not necessarily reversible either.

Being Patient: How do we diagnose vascular dementia?

Sabbagh: Vascular dementia is really diagnosed through the clinical story of sudden abrupt worsening and cognition that then plateaus and then abruptly gets worse and then plateaus. [That’s] what’s called a stepwise decline and MRI changes. A lot of people have a little bit of change on their MRI, and people overcall vascular dementia when it’s actually not just age-related findings, but if you have a lot of changes on your MRI, you might think about vascular dementia. 

Being Patient: This is my confusion with my own mom. When she was first experiencing problems, she was diagnosed with Alzheimer’s, but they found little tears on her brain, bleeds on her brain, which could be normal aging, right? What puzzled me in the earlier stage was that the progression was up and down. This happened for a long time. Is that typical of Alzheimer’s?

Sabbagh: No, that’s not. That’s more typical for vascular or Lewy Body. 

Being Patient: That’s what I thought. To this day, I have asked, “Does she actually have vascular dementia?” But then, do all of these dementias meet when you’re in a later stage?

Sabbagh: We know that pure disease is rare. Pure Alzheimer’s is where you have plaques and tangles and nothing else—there’s only a third of patients that [have what we] would call Alzheimer’s. The majority of them have other things like vascular, like alpha-synuclein, which is the Lewy body they had. In other words, most dementias overlap. Even vascular dementia, 90 percent of the time, have amyloid plaques and tangles in their brain. Pure vascular dementia, where they just have strokes and no plaques and tangles, is relatively uncommon. So yes, they do converge.

“We know that pure disease is rare. Pure Alzheimer’s is where you have plaques and tangles and nothing else—there’s only a third of patients that [have what we] would call Alzheimer’s.”

Being Patient: Does vascular dementia have a slower progression than Alzheimer’s

Sabbagh:  It’s variable.

Being Patient: What have you discovered in terms of the progression of the disease? Are there factors you see in faster progression vs. slower progression in Alzheimer’s?

Sabbagh: I will tell you that having two copies of the APOE4, clearly, once that train has left the station, they’re on the express train, and that has been really tough to see. I see a lot of patients decline very quickly if they have two copies of the APOE4. Lewy Body patients tend to progress more rapidly. If I had to predict the two groups of people that are likely to progress quickly, it would be Lewy Body patients and APOE4 double copy.

Being Patient: We have a question from our audience. For a patient diagnosed with MCI, how effective are changes in lifestyle, exercise, and diet for delaying Alzheimer’s?

Sabbagh: There are a lot of studies now suggesting that diet and exercise, particularly exercise, does slow the rate of progression, rate of decline. So, the lifestyle factors should be implemented as early as possible.

Diet is controversial, but clearly, we know that cognitive stimulation, blood pressure management, and physical exercise have enough evidence to recommend them. Diet, everybody’s on a different opinion on the diet, so there’s not enough data to give you enough studies to give official recommendations around diet. But yes, you should be making changes in the mild carb impairment that are lifestyle-directed.

Katy Koop is a writer and theater artist in Raleigh, NC.

UPDATE, 20 November 2023: As of a landmark policy change in October 2023, Medicare now also covers beta-amyloid PET scans for diagnosing Alzheimer’s disease.

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8 thoughts on “‘Don’t Let Doctors Dismiss Your Concerns:’ A Neurologist on Diagnosing Dementia

  1. I just finished reading the discussion with Dr. Sabbagh in regard to diagnosing dementia. Really excellent. Would it be possible to obtain a hard copy/transcript of the discussion? My wife is dealing with what her neurologist calls MCI but getting an accurate diagnosis has been very frustrating. Thank you.

  2. All good info to know as I watch my Mom’s Health decline! She doesn’t move much and eats lots of sugar. She was diagnosed three years ago, although I saw signs 7-8 years ago! Her memory is bad, but still is able to bathe and dress herself, but has started wetting, in her shoes! Can’t convince her to wear depends, and the fight isn’t worth it! Thanks for all your work to end this disease!

  3. My Husband is 2years 5months down the line of 1st going to the GP s with cognitive impairment,he has had numerous MRI scans a lumbar puncture Tau protein detected and aweeks lumbar drain where they neglected to test for protein.He was tested daily during the hospital stay by the neurophysiologist and neuropsychologist who found no improvement with the drain.He has been referred back to the memory clinic that he first attended in November 2021 and was refused memory testing as he was involved with neurosurgery because of the hydrocephalus.He had a CT scan last week to be reviewed by the memory clinic WHEN we get an appointment to go there. In the meanwhile his symptoms have worsened.Advice please as Could Be Alzheimer’s but no definite diagnosis Thank you his wife Jo xxxx

  4. Muy interesante la entrevista, se requiere dar mayor atención a la salud mental, a nivel mundial, es muy precaria la importancia que los gobiernos dan a este problema que va creciendo exponencialmente.

    Felicidades por ésta entrevista!

  5. I found this incredibly interesting and helpful. It was presented in a logical and easy to understand format. It addressed some questions I’ve had, and gave me new things to consider. I am so glad I came across it.

  6. I am 85 y/o and have been having memory problems for approx 2 yrs. Through an MD I am following Dr. Bredesen’s advise regarding multiple supplements, etc. I am not any better – I believe I am gradually getting worse. Do you have any comments? Thank you.

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