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1.
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Determine whether MCI is due to AD
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2.
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Differentiate AD from non-AD dementia (for example, frontotemporal lobar degeneration), particularly in early age-at-onset patients
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3.
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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)
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4.
|
Differentiate AD from nondegenerative cognitive decline (for example, depression, substance abuse)
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5.
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Determine whether AD is present in patients with advanced dementia and no reliable history
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6.
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Identify whether AD is present in focal cortical syndromes (for example, posterior cortical atrophy, primary progressive aphasia, corticobasal syndrome)
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7.
|
Differentiate cerebral amyloid angiopathy from intracranial hemorrhage due to small-vessel vasculopathy
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Unlikely to have clinical utility
|
|
1.
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Initial investigation of cognitive complaints (in the absence of a detailed neurologic evaluation and cognitive testing)
|
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2.
|
Differentiate AD from other amyloid-beta-associated dementia (for example, dementia with Lewy bodies, cerebral amyloid angiopathy)
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3.
|
Differentiate between AD clinical variants (for example, classic amnestic AD vs. posterior cortical atrophy or logopenic variant primary progressive aphasia)
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4.
|
Differentiate between non-AD causes of dementia (for example, molecular subtypes of frontotemporal lobar degeneration)
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Utility for research only
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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)
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2
|
Selection of candidates for anti-amyloid treatment trials (AD, MCI, preclinical)
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3
|
Study of the natural evolution of amyloid burden and its role in the pathophysiology of AD and other dementias
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4
|
Potential surrogate marker for anti-amyloid therapies
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