Amyloid and tau PET scans of my brain 

In 2015 I volunteered for a longitudinal study of a then new tau-PET scan using the radioactive tracer [¹⁸F]-AV1451. It has since been approved for commercial use under the name Flortaucipir. Along with the tau PET scan, I had an amyloid PET scan using the tracer ¹¹C-PiB, a high-resolution MRI scan, and extensive cognitive testing.  All of these tests have been repeated in 2018 and 2022. Let’s look at the amyloid PET first.

In 2015, there was a moderate amount of amyloid in cortical regions of the brain, especially in the prefrontal and frontal lobes. At this time, I had mild, subjective feelings of cognitive impairment, but my objective cognitive testing was still normal. In 2016 I enrolled in a clinical trial of the anti-amyloid monoclonal antibody aducanumab. For 18 months I received monthly infusions of what turned out to be placebo. In September 2017, I entered an open label extension study during which I received active drug every month. Just before Christmas, I developed the most severe headache of my life combined with severe confusion and extremely high blood pressure requiring ICU care. I have discussed this severe episode of ARIA (amyloid-related imaging abnormalities) in chapter 13 of my book A Tattoo on my Brain and in a case report published in Alzheimer’s & Dementia. As shown in the MRI below, I had evidence of swelling in multiple areas throughout my brain. 

It took about six months to fully recover from the ARIA episode. I returned to UCSF for another set of PET scans about nine months after the ARIA event.  As seen in the amyloid PET scan above, in 2018 there actually was less amyloid seen in my brain.  As we now know, aducanumab and similar drugs are actually quite effective at removing amyloid from the brain, and after just four doses, there was less in my brain. However, that benefit was not sustained. In the last amyloid PET scan above shows, by last month (2022) the amyloid had returned and progressed.

What about tau?  Recall that tau is the abnormal protein found in neurofibrillary tangles of Alzheimer’s disease. It can first be detected a few years before the onset of cognitive impairment.  As shown in my tau PET scans below, in 2015 when I had very mild cognitive impairment, there was just the beginning of tau deposition in the anterior temporal lobes, especially on the left. In 2018 and again in 2022, the tau had spread on both sides. This is the part of the brain where short term memory is consolidated into long term memory, so it is not surprising that my cognitive testing shows worsening of verbal memory. But the rest of my brain still looks pretty good, both on the tau PET scans and in the cognitive tests.

What’s my take home message?  I am very encouraged by these studies. My Alzheimer’s disease is progressing very slowly. Damage to my brain has been limited mostly to the temporal lobes and olfactory centers.  Extensive cognitive testing now puts me in the border zone between mild cognitive impairment and mild dementia.  I am still largely independent in my activities of daily living, although I now rely on my wife to handle the family finances. I can still read, and I write almost every day. I don’t know exactly why my Alzheimer’s is progressing so slowly.  Perhaps I have some unidentified genetic factor that counteracts the effects of my two APOE-4 alleles.   Perhaps I have enough cognitive reserve to keep my brain functioning for a while longer.  Perhaps the lifestyle changes I adopted are making a difference. Maybe the four doses of aducanumab did something useful (although I think it is unlikely). Whatever the cause, life is still good, and I intend to keep doing everything I can to keep it that way.