학술논문

Mild cognitive impairment with suspected nonamyloid pathology (SNAP)
Document Type
article
Author
Caroli, AnnaPrestia, AnnapaolaGalluzzi, SamanthaFerrari, Clarissavan der Flier, Wiesje MOssenkoppele, RikVan Berckel, BartBarkhof, FrederikTeunissen, CharlotteWall, Anders ECarter, Stephen FSchöll, MichaelChoo, Il HanGrimmer, TimoRedolfi, AlbertoNordberg, AgnetaScheltens, PhilipDrzezga, AlexanderFrisoni, Giovanni BWeiner, MichaelAisen, PaulPetersen, RonaldJack, Clifford RJagust, WilliamTrojanowki, JQToga, Arthur WBeckett, LaurelGreen, Robert CGamst, AnthonySaykin, Andrew JMorris, JohnPotter, William ZMontine, TomThomas, Ronald GDonohue, MichaelWalter, SarahDale, AndersBernstein, MatthewFelmlee, JoelFox, NickThompson, PaulSchuff, NorbertAlexander, GeneDeCarli, CharlesBandy, DanKoeppe, Robert AFoster, NormReiman, Eric MChen, KeweiMathis, ChetCairns, Nigel JTaylor-Reinwald, LisaShaw, LesLee, Virginia M-YKorecka, MagdalenaCrawford, KarenNeu, ScottHarvey, DanielleKornak, JohnForoud, Tatiana MPotkin, StevenShen, LiKachaturian, ZavenFrank, RichardSnyder, Peter JMolchan, SusanKaye, JeffreyDolen, SaraQuinn, JosephSchneider, LonPawluczyk, SoniaSpann, Bryan MBrewer, JamesVanderswag, HelenHeidebrink, Judith LLord, Joanne LJohnson, KrisDoody, Rachelle SVillanueva-Meyer, JavierChowdhury, MunirStern, YaakovHonig, Lawrence SBell, Karen LMorris, John CMintun, Mark A
Source
Neurology. 84(5)
Subject
Biomedical and Clinical Sciences
Clinical Sciences
Aging
Alzheimer's Disease
Neurosciences
Brain Disorders
Acquired Cognitive Impairment
Neurodegenerative
Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD)
Dementia
2.1 Biological and endogenous factors
Aetiology
Neurological
Aged
Aged
80 and over
Cognitive Dysfunction
Databases
Factual
Disease Progression
Female
Follow-Up Studies
Humans
Male
Middle Aged
Neurodegenerative Diseases
Plaque
Amyloid
Predictive Value of Tests
Alzheimer's Disease Neuroimaging Initiative
Cognitive Sciences
Neurology & Neurosurgery
Clinical sciences
Language
Abstract
ObjectivesThe aim of this study was to investigate predictors of progressive cognitive deterioration in patients with suspected non-Alzheimer disease pathology (SNAP) and mild cognitive impairment (MCI).MethodsWe measured markers of amyloid pathology (CSF β-amyloid 42) and neurodegeneration (hippocampal volume on MRI and cortical metabolism on [(18)F]-fluorodeoxyglucose-PET) in 201 patients with MCI clinically followed for up to 6 years to detect progressive cognitive deterioration. We categorized patients with MCI as A+/A- and N+/N- based on presence/absence of amyloid pathology and neurodegeneration. SNAPs were A-N+ cases.ResultsThe proportion of progressors was 11% (8/41), 34% (14/41), 56% (19/34), and 71% (60/85) in A-N-, A+N-, SNAP, and A+N+, respectively; the proportion of APOE ε4 carriers was 29%, 70%, 31%, and 71%, respectively, with the SNAP group featuring a significantly different proportion than both A+N- and A+N+ groups (p ≤ 0.005). Hypometabolism in SNAP patients was comparable to A+N+ patients (p = 0.154), while hippocampal atrophy was more severe in SNAP patients (p = 0.002). Compared with A-N-, SNAP and A+N+ patients had significant risk of progressive cognitive deterioration (hazard ratio = 2.7 and 3.8, p = 0.016 and p < 0.001), while A+N- patients did not (hazard ratio = 1.13, p = 0.771). In A+N- and A+N+ groups, none of the biomarkers predicted time to progression. In the SNAP group, lower time to progression was correlated with greater hypometabolism (r = 0.42, p = 0.073).ConclusionsOur findings support the notion that patients with SNAP MCI feature a specific risk progression profile.