Tau PET Scans in Alzheimer’s

A high-level summary of where the field stands in August 2026

By Dave McKissock

 The big picture. Tau PET is becoming an increasingly important part of the Alzheimer’s biomarker landscape. The FDA approval of Tauklarify™ (florquinitau F-18, formerly MK-6240) on August 14, 2026 is an important milestone—but it is not the beginning of FDA-approved tau PET. Tauvid™ (flortaucipir F-18) was approved in 2020. The important change is that clinicians in the United States now have two FDAapproved tau PET tracers.

 Why does that matter? Amyloid and tau provide different pieces of the Alzheimer’s story. Amyloid can accumulate many years before symptoms, while the amount and distribution of tau—particularly as it extends into the neocortex—are more closely associated with cognitive impairment and disease progression. Tau PET gives researchers and clinicians a way to see where aggregated tau pathology is located in a living brain.

 A Simple Way to Think About the Biomarkers

 These tests are not necessarily competitors. They may increasingly become complementary pieces of the same diagnostic and staging puzzle.

 What Tau PET Adds

• Tau PET can detect tau accumulation across the Alzheimer’s continuum and can show patterns of tau spread that broadly resemble the progression described by Braak staging.

• In simple terms, earlier tau is often concentrated in medial-temporal regions involved in memory, while more extensive disease can involve the neocortex—the outer layer of the brain involved in language, reasoning, perception, planning and complex thinking.

• This spatial information is one of tau PET’s major advantages. A blood test can indicate that Alzheimer’s-related biology is present, but it cannot currently show where the tau pathology is located in the brain.

• Research with MK-6240 has shown that tau PET can track changes in tau over time and that increasing tau burden is associate

 Two FDA-Approved Tau PET Tracers

Tauvid™ (flortaucipir F-18) was the first FDA-approved tau PET tracer, in 2020. It is designed to estimate the density and distribution of aggregated tau neurofibrillary tangles in adults with cognitive impairment being evaluated for Alzheimer’s disease.

 Tauklarify™ (florquinitau F-18, formerly MK-6240) became the second FDA-approved tau PET tracer on August 14, 2026. Although its clinical approval is new, the underlying research program is not: MK-6240 had been used extensively in research, including many clinical trials.

 Importantly, these are different chemical compounds—not simply two brand names for the same tracer. They have broadly similar clinical purposes, but they differ in binding characteristics, off-target signal, imaging protocols and quantitative behavior.

 Why Having Two Tracers Is Important

• Potentially greater availability: a second approved tracer may allow more imaging centers to offer tau PET.

• Choice and competition: two commercially available tracers may encourage improvements in access, production, interpretation and cost.

• More comparative research: head-to-head studies can help researchers understand how the two tracers relate to one another.

• A need for standardization: numerical results from one tracer should not automatically be treated as interchangeable with results from another.

 Does Tauklarify work better than Tauvid?

It is too early to make that claim. Comparative research has found broadly similar patterns of tau deposition while also finding meaningful technical differences. Some studies suggest advantages for Tauklarify in signal range or detection of early tau, but these findings do not establish overall clinical superiority.

 Where Does Tau PET Fit Clinically?

The 2025 Alzheimer’s Association/Society of Nuclear Medicine and Molecular Imaging Appropriate Use Criteria provide a useful high-level framework:

• Amyloid biomarkers are generally considered “Core 1” biomarkers that can establish the biological presence of Alzheimer’s disease.

• Tau PET is considered a “Core 2” biomarker, potentially adding information about biological stage and prognosis after Alzheimer’s biology has been established.

• Tau PET may be particularly useful in selected patients when information about tau burden or distribution could help clarify disease stage or prognosis.

 But tau PET is not a stand-alone diagnosis. A positive scan should be interpreted in the context of symptoms, cognitive testing, amyloid status, MRI findings and other biomarkers. A negative scan does not necessarily exclude very early tau pathology.

 What About Alzheimer’s Treatments?

 Tau PET may become increasingly relevant as Alzheimer’s care moves toward biological diagnosis and disease-modifying treatment. Clinical-trial analyses of anti-amyloid therapies have suggested that people with lower baseline tau burden may, as a group, obtain greater benefit from amyloid removal.

However, an important distinction: tau PET is not currently required by the FDA prescribing information for Leqembi® (lecanemab) or Kisunla® (donanemab), and tau PET is not yet established as a routine method for monitoring response to anti-amyloid treatment.

 Where Might the Field Go Next?

• Blood biomarkers such as p-tau217 may increasingly identify Alzheimer’s biology without requiring a PET scan.

• Newer blood biomarkers are being studied for their ability to provide information more closely related to established tau-tangle pathology.

• Tau PET has a unique role because it provides spatial information—showing where tau is located and how extensively it has spread.

• As the technology matures, blood biomarkers and tau PET may become complementary: blood tests for convenient detection and monitoring, and tau PET for situations where detailed biological staging or spatial information is important.

• If effective anti-tau therapies emerge, tau PET could become even more important for identifying appropriate patients and assessing biological effects of treatment.