2 The NIA–AA preclinical AD workgroup who proposed this concept operated under the assumption that the term ‘AD’ referred to the pathological condition and that clinical symptoms resulting from the pathological condition are not required in the definition of AD. Preclinical AD was a new concept, in which clinically normal individuals with biomarker evidence of AD pathology were hypothesized to be on the trajectory towards symptomatic AD. 5 Signature topographic patterns characteristic of AD 6 revealed by 18F-FDG–PET and MRI are used as evidence of AD-related neurodegeneration ( Figure 1). The biomarkers of AD-related neurodegeneration are high levels of tau in CSF, brain hypometabolism as assessed by 18F-FDG–PET and atrophy as assessed by anatomic MRI. Biomarkers of fibrillary β-amyloid deposition are high ligand retention on amyloid PET and low levels of amyloid-β 42 in the cerebrospinal fluid (CSF). 2– 5 Five biomarkers are used in the NIA–AA classification. The NIA–AA criteria rely on biomarkers to classify individuals as either amyloid-β-positive or amyloid-β-negative, and as neurodegeneration-positive or neurodegeneration-negative. SNAP was first described in a study 1 in which the National Institute on Aging–Alzheimer’s Association (NIA–AA) criteria of preclinical AD 2 were examined. Suspected non-Alzheimer disease (AD) pathophysiology (SNAP) is a biomarker-based concept denoting AD-like neurodegeneration in individuals without β-amyloidosis. In this Perspectives article we describe the available data on SNAP and address topical controversies in the field. Clinically normal and mildly impaired individuals with SNAP have worse clinical and/or cognitive outcomes than individuals with normal levels of neurodegeneration and amyloid-β biomarkers. APOE4 is underrepresented in individuals with SNAP compared with amyloid-positive individuals. SNAP is present in ~23% of clinically normal individuals aged >65 years and in ~25% of mildly cognitively impaired individuals. The term SNAP has been applied to individuals who are clinically normal for their age and to individuals with mild cognitive impairment, but is applicable to any amyloid-negative, neurodegeneration-positive individual regardless of clinical status, except when the pathology underlying neurodegeneration can be confidently inferred from the clinical presentation. Suspected non-Alzheimer disease pathophysiology (SNAP) is a biomarker-based concept that applies to individuals with normal levels of amyloid-β biomarkers in the brain, but in whom biomarkers of neurodegeneration are abnormal.
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