Neuro-imaging
Brain PET scans can now show the sticky protein clumps of Alzheimer's disease directly, and are also used to see how far a brain tumour has spread and whether radiotherapy scarring looks like tumour regrowth.
Overview
Amyloid and tau PET are the most consequential recent additions to neuro-imaging: the 2025 Appropriate Use Criteria from the Alzheimer's Association and SNMMI (updated from 2013, published simultaneously in Alzheimer's & Dementia and the Journal of Nuclear Medicine) rated 7 of 17 clinical scenarios as appropriate for amyloid PET and 5 of 17 for tau PET, chiefly assessment and prognosis of mild cognitive impairment, working up dementia of unclear cause, and determining eligibility for and monitoring response to anti-amyloid immunotherapies. Under the 2024 Alzheimer's Association diagnostic criteria, amyloid PET is a "Core 1" biomarker sufficient to establish the diagnosis, while tau PET is a "Core 2" biomarker used to stage disease once diagnosis is established.
FDG PET keeps a distinct, complementary role in distinguishing Alzheimer's disease from other dementia subtypes by its regional pattern of hypometabolism, and is also used in neuro-oncology to help separate tumour recurrence from radiation necrosis after treatment for glioma or meningioma, a distinction that is often difficult on structural MRI alone. Somatostatin receptor PET (68Ga-DOTATATE) has become the imaging standard for meningioma, matching the joint EANM/EANO/RANO/SNMMI theranostics practice guideline that also covers SSTR-ligand radionuclide therapy for meningioma.
What remains unsolved: expanded reimbursement for amyloid and tau PET has improved access in the US, but availability and payer coverage still vary widely internationally, and the AUC explicitly discourage use of these scans outside a proper dementia-specialist workup (for example, they are rated rarely appropriate for asymptomatic people who simply carry the APOE4 risk gene). Radiation necrosis after stereotactic radiotherapy remains genuinely difficult to distinguish from recurrent tumour even with modern PET tracers in a meaningful minority of cases.
Notes
top- The 2025 SNMMI/Alzheimer's Association AUC explicitly discourage amyloid or tau PET in people with no cognitive impairment, even if they carry the APOE4 risk allele, and in place of genetic testing for suspected causal mutations.
- Distinguishing radiation necrosis from tumour recurrence on PET after brain radiotherapy remains genuinely difficult in a meaningful minority of cases; no single tracer resolves it definitively.
- Coverage and access for amyloid/tau PET have expanded in the US but remain uneven internationally.