Conflicting Neuroquant MRI and Petscan

Jack16

I am have started Kisunla infusions, and after my first treatment I had a “ neuroquant MRI” in order to detect if there has been any brain hemorrhages due to the medication.

The results fortunately came back negative and the report also mentioned that I do not have brain atrophy. Other MRIs have said I have more brain shrinkage than normal for my age so I am a little confused.

I have had two Pet Scans come back positive. My neuropsychologist has told me I have MCI due to Alzheimer’s. Other cognitive tests have suggested amnestic MCI. My biomarkers are positive.

This latest MRI test has me questioning everything. Of course I am hoping that the MRI negates any other results that I have had that are positive.

I am so tired of all of the testing and trying to decipher and question results. Very tough for a micro manager!

What is the saying “denial is just another river in Egypt?”

Jack

LBC83

I understand your quandary. At the best of times, the US medical establishment can be difficult to deal with. Receiving an MCI diagnosis is one of those life-changing events that nobody wants to hear.
I had noticed a slight degradation in my memory, and given my family history of dementia, I raised this concern with Dr during my annual physical. She referred me to a center specializing in the brain, where I had numerous tests. I was diagnosed with MCI. Long story short, I just had my 12th infusion of Leqembi. I haven't paid much attention to the details from the several MRIs I've received, other than nothing that they have indicated no signs of ARIA, as that is the key reason for the MRIs. Yes, the MRIs also can provide information about brain volume, which is mildly interesting in relation to the progression of Alzheimer's. But for me, the real test is the rate of memory degradation. The point of Leqembi and Kisunla is to slow (but not stop) the rate of progression of the disease. Others have compared it to slowing a car from 60 mph to 45 mph. I don't think that is a great comparison, as anybody can easily detect that change in car speed, but it is very hard to detect small decreases in the already slow degradation rate of Alzheimer's. So I'm learning to just take one day at a time, enjoy each day as best I can, and stay involved with life by posting long commentaries on ALzConnected! I'm happy to know that I'm buying more high-quality time with my family from my bi-weekly Leqembi infusions.

Jack16

Thank you for your insightful comment.

I asked the neurologist via her portal about the results of the MRI ,which I read as negative for brain atrophy because I was in the 89% zone. I believed that to mean that I was in the top level of no atrophy, which, as she corrected me, means that 89% of people in my age group have less atrophy. Oh well, time for me to stop retrieving my results on the imaging centers portal and trying to interpret, before I see my neurologist, rather than thinking I am one!

She also explained what we are trying to attack is the amyloid plaque and the reason for the MRI is determining if their is ARIA, which,after my first Kisunla treatment, there is not.

mvanderhaar

Hi, I am 74 female, healthy and active. I recently told my GP that I was concerned about short term memory issues. She did the blood test and it came out with a .102 A---Beta-amyloid 42/40 ratio and T--p-tau 181 value of 1.21; indicator of possible alzheimer's. Just found this out yesterday and my head is spinning. Will see Dr tomorrow to discuss MRI/Cat scans. Just reaching out; also not sure what MCI refers to but I see it used in discussions. Thanks for reading!
Mary

Iris L.

Welcome Mary. The blood test you refer to is relatively recent. Usually a diagnosis of Alzheimer's Disease is made after ruling out all possible medical causes of memory loss, such as nutritional deficiencies or hormonal disorders. A search is made for a history of head trauma, depression, and the use of prescription and over-the-counter drugs that have memory loss as a side effect. Plus you should have extensive neurocognitive testing to determine the status of your memory, cognition and other brain functions. Imaging studies search for old strokes or tumors. Then you must see a decline in cognitive functiining over a period of time. It takes time to do all these tests.

MCI refers to mild cognitive impairment. This refers to cognitive changes that are of concern, but that do not meet the criteria for dementia. MCI may be due to medical or other causes. Thus, MCI may be treated and resolved for some patients. In some cases, no specific cause is found, and the MCI may remain unchanged over time. For other patients, MCI is the early stage of Alzheimer's Disease. But no one knows until there is progression. With the new medications such as Lequembi, doctors are trying to delay progression proactively. It is best to work with a neurologist who regularly diagnoses and treats the dementias, because you need someone with knowledge and experience.

Please keep us updated on what is happening with you, Mary.

Iris

LBC83

While the post from Iris outlines what has been the typical process for an Alzheimer's Diagnosis in the past, Mary's story is part of the new wave of of diagnosis. Eisai (Japanese publicly traded company that developed Leqembi), has much information on their website about their future plans for Leqembi. Specifically, they indicate their long-term desire is that patients can be initially diagnosed via the new blood test mentioned by Mary. This new revolutionary technique upends what previously has been the long process with neurologists. As I understand the concept, just like your GP can diagnose high cholesterol and order medication based on blood work, a GP can now diagnose Alzheimer's via blood work. As Mary notes, the next step would be an MRI. Based on the MRI results, I presume Mary's GP could write a prescription for Leqembi. All without ever having memory tests, or seeing a neurologist. Welcome to the new world. Below is a chart from an Eisai presentation I found on the internet explaining their view of the old process (top part) and the new process (bottom part). PCP stands for Primary Care Physician

paperrockscissors

Many neurologists would at least add one more step in the new paradigm (which isn't approved anyway by many because the presence of AB doesn't always lead to Alzheimer's). The step they would add is genetic testing for the ApoE4 variant that raises risk of late stage Alzheimer's. The risk of ARIA his higher in these individuals, and ApoE4 is quite common. I would not myself take one of these new drugs due to having ApoE4. The small, short term benefit isn't worth the risk to me.

South Dakota Dave

I have had 27 Leqembi infusions as of Jan 2025. I have one APOE 4 gene and have no issues with it: Mayo Clinic routinely moves forward with APOE 4. Of course anything is possible. So far Alzheimer's has been "winning" but the new infusions have made inroads, Leqembi has recently shown 14% greater amyloid removal.

LBC83

I am behind South Dakota Dave, as I have only had 16 Leqembi infusions as of Jan 2025. I also have one APOE4 gene, and have also had no issues with Leqembi.

My Dec 2024 post included a diagram illustrating the old & new paradigms regarding who prescribes Leqembi and the process for the prescription. The main point of the diagram is that with the anticipated large number of people who may be diagnosed with AD in the next decade, combined with the low supply of Neurologists, results in in balance between supply & demand (to utilize economic principals). A proposed solution is to allow Primary Care Physicians to prescribe Leqembi, after cognitive testing by experts and a blood test confirming the presence of amyloid plaque.

With regards to the earlier comments from paperrockscissors, regardless of whether a primary care doctor or a neurologist is prescribing Leqembi, there is the danger of ARIA. This is noted in the diagram (labeled "ARIA monitoring"). And yes, clinical trials with Leqembi did show higher incidences of ARIA for those with both APOE genes. The trade-off seems to be accepting a fast cognitive decline with standard Alzheimer's and no Leqembi treatments or accepting some risk of ARIA with Leqembi to slow the cognitive decline. Both of my parents had dementia (it is unknown whether they specifically had Alzheimer's), so I have first hand experience witnessing the eventual state of those with Alzheimer's. For me, it was a very easy decision to start on Leqembi. Part of my decision was also based on a hope that in the next couple of years, anti-tau drugs will come to market. Two anti-tau drugs are currently undergoing Phase 3 clinical trials, and the drugs are used in combination with Leqembi. If either of these drugs prove useful in greatly slowing the progression of Alzheimer's, then I'm hoping they will receive FDA approval in time to help me in my situation.

gsergenian

I am leaning towards taking Leqembi. I am an active, healthy 85-year-old woman. I have had all the testing except a PET scan, but am scheduled for that.

However, I just saw this article in the NYT that gives me pause. It states that there has been fraud and misconduct in the research about Alzheimer's treatment, including the amyloid hypothesis.

https://www.nytimes.com/2025/01/24/opinion/alzheimers-fraud-cure.html?unlocked_article_code=1.rk4.zQ-K.nivpx06Hkyym&smid=url-share