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In‐vivo characterization of progressive amnestic syndrome due to suspected neurodegenerative non‐Alzheimer’s disease
Author(s) -
Bailly Laurent,
Villain Nicolas,
Houot Marion,
Hourregue Claire,
Paquet Claire,
Leroy Melanie,
Lebouvier Thibaud,
Dubois Bruno,
Epelbaum Stéphane
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.039587
Subject(s) - atrophy , neurodegeneration , medicine , episodic memory , psychology , cognitive decline , snap , dementia , alzheimer's disease , amnesia , disease , pathology , neuroscience , cognition , psychiatry , computer graphics (images) , computer science
Background Neuropathological bases of suspected non‐Alzheimer’s disease pathophysiology (SNAP) have recently been identified as frequent causes of progressive isolated amnestic non Alzheimer’s disease (AD) neurodegenerative diseases 1,2 . Nonetheless, their in‐vivo profiles have so far been only poorly characterized. The goal of this study is to specify their clinical, neuroimaging profile and evolution, compared to patients with amnestic AD and cognitively normal subjects. Methods We retrospectively selected patients with progressive amnestic syndrome of hippocampal type 3 , signs of neurodegeneration (elevated CSF t‐ tau concentration and/or brain hypometabolism and/or atrophy) and normal CSF Amyloid values (Aβ42 concentration ; Aβ40/42 ratio if available) from 3 tertiary memory centers (amnestic SNAP). They were compared to patients with prodromal typical (amnestic) AD (without impairment of instrumental functions, MMSE >20, elevated CSF p‐tau and abnormal CSF Amyloid values) and cognitively normal controls with normal CSF Amyloid values. We compared clinical data and neuropsychological tests between amnestic SNAP and the two other groups. Results 25 patients with amnestic SNAP (median age=74.7), 24 amnestic AD (median age=71) and 35 controls (median age=75) were included. At baseline, controls had better global cognitive performances (MMSE=29 vs. 27 vs. 25 respectively, p<0.001) as well as verbal fluency performances than amnestic SNAP and amnestic AD but no significant difference were found between amnestic SNAP and AD (p=0.096). Executive functioning was significantly different between controls, amnestic SNAP and AD (FAB=17, 16 and 14 respectively, p<0.001) and there was a significant difference between amnestic SNAP and AD (p=0.034). We found no other significant difference between amnestic SNAP and AD: neither regarding memory performances (FCSRT) nor other cognitive functions (language, visuo‐spatial abilities). Conclusion Patients with amnestic SNAP show a weaker impairment in executive functions than patients with prodromal amnestic AD, highlighting a specific identifiable baseline neuropsychological pattern. This work will be completed by the analysis of clinical evolution, and the pattern of brain atrophy and brain metabolism that will be available at the time of AAIC. References: 1. Nelson et al. (2019). Brain, 142(6):1503‐1527. 2. Crary et al. (2014). Acta Neuropathol. 2014 Dec;128(6):755‐66. 3. Dubois B. & Albert M (2004). Lancet Neurol, 3 (4), 246‐8.