A PET scan in someone with Alzheimer’s disease can reveal three distinct types of abnormalities in the brain: the accumulation of amyloid plaques, the spread of tau protein tangles, and regions of reduced glucose metabolism. Together, these findings give clinicians a window into the biological processes driving cognitive decline — often before a person has any noticeable symptoms. For example, an amyloid PET scan performed on a 60-year-old with mild memory complaints might show significant plaque buildup in the cortex years before a formal Alzheimer’s diagnosis would otherwise be made.
This article covers what each type of PET scan detects, how results are interpreted, what the findings mean for treatment decisions, and the important limitations of this technology. PET imaging has become one of the most powerful diagnostic tools in Alzheimer’s medicine, but it is not a simple yes-or-no test. Understanding what a PET scan actually shows — and what it cannot tell you on its own — is essential for families and patients navigating a potential diagnosis. The results must always be interpreted alongside a full clinical history, cognitive testing, and other biomarkers.
Table of Contents
- What Does an Alzheimer’s PET Scan Actually Detect in the Brain?
- How Amyloid PET Findings Are Interpreted and What They Mean
- What Tau PET Reveals — and Why Researchers Consider It the Best Predictor of Decline
- When PET Scans Are Recommended — and When They Are Not
- Limitations and Caveats Every Patient and Family Should Know
- How PET Compares to Other Alzheimer’s Diagnostic Tools
- Where Alzheimer’s PET Imaging Is Headed
- Conclusion
- Frequently Asked Questions
What Does an Alzheimer’s PET Scan Actually Detect in the Brain?
There are three main types of PET scans used in Alzheimer’s evaluation, and each targets something different. An amyloid PET scan detects sticky protein deposits called amyloid plaques that accumulate in cortical brain regions. These plaques are one of the defining hallmarks of Alzheimer’s disease, and amyloid PET is capable of identifying this buildup years before a person develops memory problems or behavioral changes. Three FDA-approved tracers are currently available for amyloid imaging: 18F-florbetapir (sold as Amyvid), 18F-florbetaben (Neuraceq), and 18F-flutemetamol (Vizamyl). Tau PET scans detect a different pathological feature — tau tangles, which are twisted fibers of tau protein that accumulate inside neurons and disrupt their function. Unlike amyloid, which tends to spread relatively diffusely, tau tangles follow a predictable pattern called Braak staging: they typically begin in memory-related areas of the brain and spread outward as the disease progresses.
This staging pattern makes tau PET particularly useful for tracking how far the disease has advanced. The FDA approved the first tau-specific tracer in 2020, and several additional tracers — including 18F-flortaucipir, 18F-MK6240, 18F-RO948, and 18F-PI2620 — are now part of the clinical and research landscape. The third type, FDG-PET, takes a different approach entirely. Rather than looking for specific proteins, it measures how efficiently the brain uses glucose. Neurons that are damaged or dying consume less glucose, and in Alzheimer’s patients, FDG-PET consistently shows reduced metabolism in the temporal and parietal lobes — regions central to memory and spatial reasoning. This metabolic signature is also useful for distinguishing Alzheimer’s from other forms of dementia. Frontotemporal dementia, for instance, shows a different metabolic pattern in FDG-PET imaging, which can help guide diagnosis when clinical symptoms are ambiguous.
How Amyloid PET Findings Are Interpreted and What They Mean
When a radiologist reads an amyloid PET scan, they are looking for whether amyloid plaque burden is elevated in cortical brain regions. A positive scan indicates meaningful amyloid accumulation; a negative scan makes Alzheimer’s disease substantially less likely as the cause of someone’s cognitive symptoms. This distinction has real clinical weight. A patient presenting with memory decline who has a negative amyloid scan may warrant investigation for other causes — vascular dementia, depression, medication side effects, or another neurological condition. However, a positive amyloid scan does not equal an Alzheimer’s diagnosis on its own.
This is one of the most important caveats surrounding this technology. Some cognitively normal older adults have elevated amyloid on PET imaging and never develop dementia, or develop it only years or decades later. Amyloid accumulation is necessary for Alzheimer’s, but it is not always sufficient to produce cognitive symptoms. This means a positive result has to be placed in context — how old is the patient, what are their cognitive test results, does their clinical presentation match? The interpretation standards for amyloid PET are also still evolving. The January 2025 guidance update from the Alzheimer’s Association and the Society for Nuclear Medicine and Molecular Imaging acknowledges that imaging results require careful clinical integration. The guidance specifically recommends that PET scans be ordered only when results will directly affect care decisions — not as a routine screening tool or out of general curiosity about brain health.
What Tau PET Reveals — and Why Researchers Consider It the Best Predictor of Decline
Tau PET has emerged as arguably the most clinically informative of the Alzheimer’s PET modalities. According to research from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), tau PET is currently the best predictor of cognitive decline among the major Alzheimer’s biomarkers. This is because tau tangle distribution correlates more closely with actual neuron loss and cognitive impairment than amyloid burden does. A person can have a heavy amyloid load and still maintain relatively preserved cognition; tau accumulation in key regions is more reliably tied to when and how severely symptoms emerge. The Braak staging system that governs tau spread gives PET scans a kind of disease timeline. In early Braak stages, tangles are confined largely to the entorhinal cortex and hippocampus — regions governing memory formation.
As staging advances, tau spreads into association cortices, then more broadly across the brain. A tau PET scan that shows spread into parietal and frontal regions suggests a more advanced stage of disease than one confined to medial temporal structures. For a clinician trying to counsel a family about prognosis or about eligibility for treatment, this information is meaningful in a way that many other tests cannot match. A practical example: a 68-year-old with mild cognitive impairment might undergo both amyloid and tau PET as part of a workup for a clinical trial. The amyloid scan is positive. The tau scan shows tangles limited to the hippocampus and entorhinal cortex. This pattern is consistent with an early stage of Alzheimer’s-related pathology — still in a range where disease-modifying therapies might have the greatest potential impact, and before the broader tau spread associated with more severe cognitive loss.
When PET Scans Are Recommended — and When They Are Not
Updated guidance published in January 2025 by the Alzheimer’s Association and the Society for Nuclear Medicine and Molecular Imaging lays out specific circumstances in which amyloid and tau PET is appropriate. The strongest evidence supports use in three main scenarios: evaluating someone with mild cognitive impairment whose diagnosis is uncertain, resolving an ambiguous dementia diagnosis when clinical and cognitive data alone are insufficient, and screening patients for eligibility for amyloid-lowering drug treatments such as lecanemab (brand name Leqembi). That last use case — treatment eligibility — has become increasingly significant. Lecanemab and similar anti-amyloid therapies are approved for patients with confirmed amyloid pathology and early-stage disease. A negative amyloid PET scan would disqualify someone from receiving these treatments, while a positive scan is a prerequisite.
This has given amyloid PET a direct clinical role beyond diagnosis: it is now part of the gatekeeping process for a class of drugs that can only benefit patients in a specific biological category. The tradeoff is cost and access. PET scans are expensive and not universally covered by insurance, and access to specialized nuclear medicine facilities with the appropriate tracers is not uniform. This creates a disparity where the patients and families who might benefit most from early imaging — those in rural areas, those with limited coverage — are least likely to receive it. The 2025 guidance does not resolve this structural problem, but it does attempt to prevent overuse of scans in situations where results would not change clinical decisions, which at minimum preserves resources for cases where the benefit is clearer.
Limitations and Caveats Every Patient and Family Should Know
The most important limitation of PET scanning in Alzheimer’s is that no single scan is diagnostic on its own. A positive amyloid scan in someone with significant cognitive decline, a matching clinical history, and abnormal cognitive test scores builds a strong case for Alzheimer’s disease. The same positive scan in someone who is cognitively normal and in their 50s is far harder to interpret — it may represent presymptomatic Alzheimer’s, a risk factor, or something that never progresses to clinical disease during that person’s lifetime. Tau PET, despite its predictive power, also carries interpretive complexity. The tracers used for tau imaging can sometimes bind nonspecifically, producing signals that are not from tau tangles. Off-target binding in certain brain regions can complicate image reading.
The field is actively working on tracer development and standardized interpretation criteria, but these are still evolving. Families receiving tau PET results should ask their physician or neurologist specifically about how confident the reading is and what, if any, ambiguity remains. There is also the psychological dimension. Receiving a positive PET result — particularly an amyloid scan suggesting disease years before symptoms — can cause significant anxiety and distress. Genetic counselors and dementia specialists are typically involved when presymptomatic testing is being considered, especially in the context of clinical trials. The knowledge that amyloid is accumulating in the brain is meaningful information, but it does not come with certainty about timeline or ultimate severity, and that uncertainty can be difficult to live with.
How PET Compares to Other Alzheimer’s Diagnostic Tools
Before PET imaging became available, Alzheimer’s pathology could only be confirmed at autopsy. PET has shifted this fundamentally, allowing in vivo detection of the biological hallmarks that define the disease. However, PET is not the only modern tool available.
Cerebrospinal fluid (CSF) testing through lumbar puncture can also detect amyloid and tau protein levels, and blood-based biomarker tests — particularly plasma phospho-tau 217 — have shown strong performance in research settings and are increasingly available in clinical practice. Blood tests are less expensive and less invasive than PET imaging, and for some patients they may provide sufficient information without the cost and logistics of a scan. The practical comparison looks something like this: a blood-based biomarker test might confirm amyloid positivity with high probability, while a follow-up tau PET provides the detailed regional information needed for staging and prognosis. Rather than replacing each other, these tools are increasingly used in combination — with PET reserved for cases where lower-cost tests leave genuine clinical uncertainty.
Where Alzheimer’s PET Imaging Is Headed
PET imaging technology and the tracers used with it continue to develop rapidly. Researchers are working to improve tau tracer specificity, reduce off-target binding, and develop tracers that target additional Alzheimer’s-related proteins such as alpha-synuclein and TDP-43 — pathologies that frequently co-occur with Alzheimer’s and complicate clinical presentation. There is also growing interest in using longitudinal PET imaging — scanning the same patient over time — to track disease progression and treatment response in clinical trials.
The integration of PET data with artificial intelligence analysis is another area of active development. Machine learning tools that can extract more information from PET images — quantifying amyloid burden more precisely, mapping tau spread in three dimensions, or predicting rate of cognitive decline — may eventually make PET results more actionable and easier to communicate to patients and families. For now, the technology is powerful but requires skilled human interpretation. As more people gain access to amyloid-lowering treatments, the demand for PET imaging to confirm eligibility is likely to increase, which will push both the clinical and insurance infrastructure to keep pace.
Conclusion
A PET scan in someone with Alzheimer’s can show amyloid plaque accumulation, tau tangle distribution following a predictable staging pattern, and reduced glucose metabolism in key cognitive regions — each providing different information about the disease process. Amyloid PET can detect pathology before symptoms appear; tau PET is currently the strongest predictor of cognitive decline; FDG-PET helps distinguish Alzheimer’s from other dementias. As of 2025, updated clinical guidance recommends these scans specifically when results will change care decisions, including assessment for eligibility for amyloid-lowering therapies like lecanemab.
No PET scan should be read in isolation. The results must be integrated with clinical history, cognitive testing, and other biomarker data to be meaningful. For families navigating a potential Alzheimer’s diagnosis, the most useful next step is a conversation with a neurologist or dementia specialist who can determine whether PET imaging is appropriate for the specific clinical situation — and who can interpret the results within the full context of the patient’s health.
Frequently Asked Questions
Can a PET scan definitively diagnose Alzheimer’s disease?
No. A PET scan cannot diagnose Alzheimer’s on its own. Results must be interpreted alongside cognitive testing, clinical history, and other biomarkers. A positive amyloid scan supports the diagnosis but is not sufficient by itself.
Can a PET scan detect Alzheimer’s before symptoms appear?
Yes. Amyloid PET in particular can detect plaque accumulation in the brain years before a person develops noticeable memory or cognitive symptoms. This presymptomatic detection is one of the technology’s most significant capabilities.
Is amyloid PET covered by Medicare or insurance?
Coverage has historically been limited, though this has been evolving as amyloid-lowering treatments become available and clinical criteria become clearer. Patients should check with their insurer and discuss costs with their physician before scheduling.
What is the difference between amyloid PET and tau PET?
Amyloid PET detects sticky amyloid protein plaques that accumulate outside neurons. Tau PET detects tau protein tangles that form inside neurons. Both are hallmarks of Alzheimer’s, but tau distribution correlates more closely with actual cognitive decline and can help indicate disease stage.
Is a PET scan the same as an MRI or CT scan?
No. MRI and CT scans show brain structure — they can detect atrophy or rule out stroke or tumors, but they cannot detect amyloid or tau proteins. PET scans use radioactive tracers to reveal biological activity and specific protein accumulation, making them a fundamentally different type of imaging.
Who should consider getting an Alzheimer’s PET scan?
Current guidance supports PET imaging for people with mild cognitive impairment of uncertain cause, those with an ambiguous dementia diagnosis, and those being evaluated for eligibility for amyloid-lowering drug treatments. It is not recommended as a routine screening tool for the general population.
