Potential clinical utility | |
---|---|
1. | Determine whether MCI is due to AD |
2. | Differentiate AD from non-AD dementia (for example, frontotemporal lobar degeneration), particularly in early age-at-onset patients |
3. | Determine whether AD copathology is present in patients with cognitive impairment and other known neurologic disease (for example, Parkinson's disease, stroke/vascular disease, multiple sclerosis, epilepsy, HIV) |
4. | Differentiate AD from nondegenerative cognitive decline (for example, depression, substance abuse) |
5. | Determine whether AD is present in patients with advanced dementia and no reliable history |
6. | Identify whether AD is present in focal cortical syndromes (for example, posterior cortical atrophy, primary progressive aphasia, corticobasal syndrome) |
7. | Differentiate cerebral amyloid angiopathy from intracranial hemorrhage due to small-vessel vasculopathy |
Unlikely to have clinical utility | |
1. | Initial investigation of cognitive complaints (in the absence of a detailed neurologic evaluation and cognitive testing) |
2. | Differentiate AD from other amyloid-beta-associated dementia (for example, dementia with Lewy bodies, cerebral amyloid angiopathy) |
3. | Differentiate between AD clinical variants (for example, classic amnestic AD vs. posterior cortical atrophy or logopenic variant primary progressive aphasia) |
4. | Differentiate between non-AD causes of dementia (for example, molecular subtypes of frontotemporal lobar degeneration) |
Utility for research only | |
1 | Testing and longitudinal follow-up of asymptomatic or subjective cognitive impairments not meeting MCI criteria or at-risk individuals (for example, gene mutation carriers, family history of AD, apolipoprotein E ε4 allele) |
2 | Selection of candidates for anti-amyloid treatment trials (AD, MCI, preclinical) |
3 | Study of the natural evolution of amyloid burden and its role in the pathophysiology of AD and other dementias |
4 | Potential surrogate marker for anti-amyloid therapies |