How to Understand Your Alzheimer's Blood Tests and PET Scan Results
Looking back at the list of 20 questions I had for Dr. Frechette during the first several months of testing, none of them even asked how to read the lab reports themselves. Looking back now, I realize that understanding the reports became one of the most important parts of the process for me. So I thought I would include the two types of reports I found most useful to learn how to read: the blood tests and the amyloid PET scans.
I don’t know about you, but when I first received my six pages of blood test results, I really had no idea what they were telling me. My neurologist tried to explain them, but the main message I walked away with was simply that the results suggested mild cognitive impairment.
Over the first 22 months, my neurologist ordered a blood test that I ultimately took five different times, each requiring five to eight tubes of blood. This section gets a little technical, but early on I became interested in understanding what these readings actually meant. I gradually started focusing on the ATN section of the report, which measures biomarkers in the blood that are associated with Alzheimer’s disease.
I should also mention that different laboratories present their blood test data in different ways. I can only speak from my experience with Labcorp reports.
This is how I kept score. And this is what each item means:
Beta-amyloid 42/40 Ratio
The beta-amyloid 42/40 ratio is a blood biomarker used to help detect amyloid plaque buildup associated with Alzheimer's disease. Beta-amyloid proteins are naturally produced in the brain when a larger protein is broken down. Two important forms are beta-amyloid 40 (Aβ40), which is common and usually remains dissolved, and beta-amyloid 42 (Aβ42), which is slightly longer and much more likely to stick together and form plaques.
In Alzheimer’s disease, Aβ42 begins depositing into plaques in the brain. As this happens, less Aβ42 remains circulating in the blood relative to Aβ40. Rather than relying on the raw amount of Aβ42 alone, laboratories compare Aβ42 to Aβ40 by calculating the Aβ42/40 ratio. Using the ratio improves accuracy because it compensates for natural differences in amyloid production, blood chemistry, and sample handling between individuals.
A lower ratio generally suggests a greater likelihood of amyloid plaque accumulation in the brain, while a higher ratio suggests less evidence of amyloid pathology. In commonly used ATN blood testing, a ratio above about 0.102 is typically considered amyloid negative, while a ratio below that level is considered amyloid positive, although exact cutoffs vary by laboratory.
As you can see from my chart before I started Leqembi and just after my first 2 infusions my 42/40 ratio indicated Alzheimer’s. Eight months later those biomarkers were in the normal range.
The ratio is an important part of the ATN framework used in Alzheimer’s evaluation. In this system, “A” refers to amyloid biomarkers such as the Aβ42/40 ratio, “T” refers to tau biomarkers like p-tau181 or p-tau217, and “N” refers to markers of neurodegeneration such as NfL. An abnormal ratio alone does not diagnose Alzheimer’s disease, but it can indicate that amyloid changes associated with the disease may already be occurring, often years before symptoms become obvious. Blood-based amyloid testing has become increasingly important with the development of anti-amyloid treatments such as Leqembi and Kisunla, because these therapies are intended for patients with confirmed amyloid pathology.
Tau 181 – Tau 217
Now let’s talk about tau. Until recently I assumed this biomarker was related to tau tangles that are on the inside of neurons. I was wrong.
Blood tests used in the ATN framework for Alzheimer's disease can now measure abnormal forms of tau protein that are associated with the disease process occurring in the brain. Tau is normally a healthy protein that helps support the internal structure of neurons. In Alzheimer’s disease, however, tau becomes abnormally altered through a chemical process called phosphorylation. These altered forms are known as phosphorylated tau, or “p-Tau,” and can eventually contribute to the formation of the characteristic tau tangles seen in Alzheimer’s disease.
Two important blood biomarkers are p-Tau181 and p-Tau217. The numbers refer to the exact location on the tau protein where the abnormal phosphorylation is measured. Elevated p-Tau181 was one of the first useful blood biomarkers for Alzheimer’s disease and is associated with amyloid plaque buildup, early Alzheimer’s-related brain changes, and increased risk of cognitive decline. More recently, p-Tau217 has emerged as one of the most accurate blood indicators of Alzheimer’s pathology. Higher levels of p-Tau217 correlate strongly with amyloid positivity on PET scans, the development of tau pathology, and progression toward symptomatic Alzheimer’s disease. Many studies suggest that p-Tau217 becomes abnormal earlier and tracks disease progression more accurately than p-Tau181.
Although these blood tests measure abnormal tau activity, they do not directly measure the actual tau tangles inside the brain. Tau tangles are microscopic structures located within brain tissue and currently cannot be directly detected through a simple blood test. Instead, blood tests detect small amounts of abnormal phosphorylated tau that leak from affected neurons into the bloodstream. These measurements act as indirect biomarkers that suggest the brain may be developing tau-related pathology. Direct visualization of tau tangles still generally requires specialized tau PET imaging or examination of brain tissue (that we don’t want to do). As a result, the ATN blood test is best understood as a tool for estimating the likelihood of Alzheimer’s-related biological changes rather than directly measuring the physical tangles themselves. (Figdore & Piura, 2025)
You may notice on my chart the p-tau217 was not part of my blood test in early 2024. Science is changing rapidly finding better ways to measure Alzheimer’s.
NfL Plasma
Neurofilament Light Chain, usually called NfL, is a protein that helps support and stabilize nerve cells in the brain and nervous system. You can think of it as part of the internal framework that keeps neurons healthy and functioning properly.
When nerve cells become damaged or die, small fragments of NfL leak out of the cells and enter the cerebrospinal fluid and eventually the bloodstream. A blood test can then measure how much NfL is present in the plasma. In general, higher levels of plasma NfL suggest that more nerve cell injury is occurring somewhere in the nervous system.
Doctors and researchers use plasma NfL mainly as a way to estimate the amount of ongoing brain-cell damage. It can help track whether a disease is progressing, distinguish normal aging from more serious neurodegeneration, and monitor whether damage is becoming worse over time.
An important limitation, however, is that NfL is not specific to Alzheimer’s disease. Elevated NfL levels can appear in many different neurological conditions, including other forms of dementia, Parkinson’s disease, Multiple sclerosis, Amyotrophic lateral sclerosis, traumatic brain injury, and stroke.
NfL is best understood as a general marker of brain or nerve-cell injury. This test added to amyloid blood markers and p-Tau markers provide a more comprehensive result. (Gotze & Vrillon, 2024)
Though my results were within the normal range (0.00 – 11.55), my figures moved from 3.52 to 2.12 indicating even less cell damage over an 18 month period.
Amyloid PET scan
This is the most accurate measure of Alzheimer’s as it tells where and how dense amyloid plaques are in our brain. I have had 2, one to confirm my diagnosis and a recent one.
When I had my first Amyloid PET scan in early 2024 imaging centers relied primarily on a simple “positive vs negative” visual interpretation, or proprietary SUVR measurements (SUVR= Tracer uptake in reference region divided by Tracer uptake in target region). The results for me was a verbal positive reading for Alzheimer’s and a picture shown earlier that doesn’t really help.
The challenge at that time was that different PET tracers, scanners, and analysis software could produce different SUVR scales. Again, scientists, thankfully, converted various SUVR measurements into a more standardized universal amyloid scale called the cl scale (Centiloid).
The centiloid scale is a standardized way to measure how much amyloid plaque is in the brain, so results are comparable across hospitals and scanners.
Be sure to record this cl number so you can compare it to your next Amyloid PET scan. It is very important and the primary reason you qualify to take Alzheimer’s drugs. This information is required by Medicare and drug insurance companies.
These are the results of my last amyloid PET scan:
The words in
EXAM DESCRIPTION:
F-18 Futementamol (Vizamy) Brain PET-CT
FINDINGS:
PET BRAIN REGIONAL ASSESSMENT:
Frontal lobes: Negative
Posterior cingulate and precuneus: Negative
Parietal convexities: Negative
Lateral temporal lobes: Negative
Striatum: Negative
Normal expect uptake is seen within the brainstem, cerebellum, and cerebral white matter.
QUANTITATIVE ASSESSMENT: The remarks in () are mine.
The cortex to cerebellar ration is 0.92 (normal <1.13)
(Ratios are always a little confusing to me.
Cortex
The outer layer of the brain
Responsible for thinking, memory, reasoning, and decision-making
This is where amyloid builds up in Alzheimer’s disease
Cerebellum
A part of the brain that usually does not accumulate amyloid
Used as a “baseline” or reference.
Think of it like comparing dust levels in two rooms:
The cerebellum is the “clean reference room”
The cortex is the room you’re checking
My cortex has no more dust than expected, so the test is normal)
Centiloid: -10.7 cm (The centiloid scale (CL) is a standardized way to measure how much amyloid plaque is in the brain, so results are comparable across hospitals and scanners.
0 centiloids = normal amyloid levels (typical of healthy young adults)
100 centiloids = heavy amyloid buildup (typical of Alzheimer’s disease)
A centiloid score of –10.7 is a reassuring, normal result and strongly argues against Alzheimer’s disease as the cause of cognitive symptoms. CL scale defines zero as the typical young adult. Another term might define zero CL as the “average” for a young cognitively normal person. To get an average of zero for a group of people some must have scores below zero and some above zero. The possibility of getting a negative CL score is below the typical young adult.)
CT HEAD
There is no evidence of acute intracranial hemorrhage, acute territorial infarction, or mass. There is mild generalized cerebral volume loss. (This would be the damage done by Alzheimer’s before Leqembi).
IMPRESSION:
Negative beta-amyloid PET examination of the brain, which makes diagnosis of Alzheimer’s disease unlikely.