Applying the ATN scheme in a memory clinic population : The ABIDE project
© 2019 American Academy of Neurology..
OBJECTIVE: To apply the ATN scheme to memory clinic patients, to assess whether it discriminates patient populations with specific features.
METHODS: We included 305 memory clinic patients (33% subjective cognitive decline [SCD]: 60 ± 9 years, 61% M; 19% mild cognitive impairment [MCI]: 68 ± 9 years, 68% M; 48% dementia: 66 ± 10 years, 58% M) classified for positivity (±) of amyloid (A) ([18F]Florbetaben PET), tau (T) (CSF p-tau), and neurodegeneration (N) (medial temporal lobe atrophy). We assessed ATN profiles' demographic, clinical, and cognitive features at baseline, and cognitive decline over time.
RESULTS: The proportion of A+T+N+ patients increased with syndrome severity (from 1% in SCD to 14% in MCI and 35% in dementia), while the opposite was true for A-T-N- (from 48% to 19% and 6%). Compared to A-T-N-, patients with the Alzheimer disease profiles (A+T+N- and A+T+N+) were older (both p < 0.05) and had a higher prevalence of APOE ε4 (both p < 0.05) and lower Mini-Mental State Examination (MMSE) (both p < 0.05), memory (both p < 0.05), and visuospatial abilities (both p < 0.05) at baseline. Non-Alzheimer profiles A-T-N+ and A-T+N+ showed more severe white matter hyperintensities (both p < 0.05) and worse language performance (both p < 0.05) than A-T-N-. A linear mixed model showed faster decline on MMSE over time in A+T+N- and A+T+N+ (p = 0.059 and p < 0.001 vs A-T-N-), attributable mainly to patients without dementia.
CONCLUSIONS: The ATN scheme identified different biomarker profiles with overlapping baseline features and patterns of cognitive decline. The large number of profiles, which may have different implications in patients with vs without dementia, poses a challenge to the application of the ATN scheme.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2019 |
|---|---|
| Erschienen: |
2019 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:93 |
|---|---|
| Enthalten in: |
Neurology - 93(2019), 17 vom: 22. Okt., Seite e1635-e1646 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Altomare, Daniele [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Amyloid beta-Peptides |
|---|
| Anmerkungen: |
Date Completed 06.02.2020 Date Revised 06.02.2020 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1212/WNL.0000000000008361 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM302046615 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM302046615 | ||
| 003 | DE-627 | ||
| 005 | 20231225105904.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231225s2019 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1212/WNL.0000000000008361 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1006.xml |
| 035 | |a (DE-627)NLM302046615 | ||
| 035 | |a (NLM)31597710 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Altomare, Daniele |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Applying the ATN scheme in a memory clinic population |b The ABIDE project |
| 264 | 1 | |c 2019 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 06.02.2020 | ||
| 500 | |a Date Revised 06.02.2020 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2019 American Academy of Neurology. | ||
| 520 | |a OBJECTIVE: To apply the ATN scheme to memory clinic patients, to assess whether it discriminates patient populations with specific features | ||
| 520 | |a METHODS: We included 305 memory clinic patients (33% subjective cognitive decline [SCD]: 60 ± 9 years, 61% M; 19% mild cognitive impairment [MCI]: 68 ± 9 years, 68% M; 48% dementia: 66 ± 10 years, 58% M) classified for positivity (±) of amyloid (A) ([18F]Florbetaben PET), tau (T) (CSF p-tau), and neurodegeneration (N) (medial temporal lobe atrophy). We assessed ATN profiles' demographic, clinical, and cognitive features at baseline, and cognitive decline over time | ||
| 520 | |a RESULTS: The proportion of A+T+N+ patients increased with syndrome severity (from 1% in SCD to 14% in MCI and 35% in dementia), while the opposite was true for A-T-N- (from 48% to 19% and 6%). Compared to A-T-N-, patients with the Alzheimer disease profiles (A+T+N- and A+T+N+) were older (both p < 0.05) and had a higher prevalence of APOE ε4 (both p < 0.05) and lower Mini-Mental State Examination (MMSE) (both p < 0.05), memory (both p < 0.05), and visuospatial abilities (both p < 0.05) at baseline. Non-Alzheimer profiles A-T-N+ and A-T+N+ showed more severe white matter hyperintensities (both p < 0.05) and worse language performance (both p < 0.05) than A-T-N-. A linear mixed model showed faster decline on MMSE over time in A+T+N- and A+T+N+ (p = 0.059 and p < 0.001 vs A-T-N-), attributable mainly to patients without dementia | ||
| 520 | |a CONCLUSIONS: The ATN scheme identified different biomarker profiles with overlapping baseline features and patterns of cognitive decline. The large number of profiles, which may have different implications in patients with vs without dementia, poses a challenge to the application of the ATN scheme | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 7 | |a Amyloid beta-Peptides |2 NLM | |
| 650 | 7 | |a Apolipoprotein E4 |2 NLM | |
| 650 | 7 | |a Biomarkers |2 NLM | |
| 650 | 7 | |a MAPT protein, human |2 NLM | |
| 650 | 7 | |a tau Proteins |2 NLM | |
| 700 | 1 | |a de Wilde, Arno |e verfasserin |4 aut | |
| 700 | 1 | |a Ossenkoppele, Rik |e verfasserin |4 aut | |
| 700 | 1 | |a Pelkmans, Wiesje |e verfasserin |4 aut | |
| 700 | 1 | |a Bouwman, Femke |e verfasserin |4 aut | |
| 700 | 1 | |a Groot, Colin |e verfasserin |4 aut | |
| 700 | 1 | |a van Maurik, Ingrid |e verfasserin |4 aut | |
| 700 | 1 | |a Zwan, Marissa |e verfasserin |4 aut | |
| 700 | 1 | |a Yaqub, Maqsood |e verfasserin |4 aut | |
| 700 | 1 | |a Barkhof, Frederik |e verfasserin |4 aut | |
| 700 | 1 | |a van Berckel, Bart N |e verfasserin |4 aut | |
| 700 | 1 | |a Teunissen, Charlotte E |e verfasserin |4 aut | |
| 700 | 1 | |a Frisoni, Giovanni B |e verfasserin |4 aut | |
| 700 | 1 | |a Scheltens, Philip |e verfasserin |4 aut | |
| 700 | 1 | |a van der Flier, Wiesje M |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Neurology |d 1951 |g 93(2019), 17 vom: 22. Okt., Seite e1635-e1646 |w (DE-627)NLM000034355 |x 1526-632X |7 nnns |
| 773 | 1 | 8 | |g volume:93 |g year:2019 |g number:17 |g day:22 |g month:10 |g pages:e1635-e1646 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1212/WNL.0000000000008361 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 93 |j 2019 |e 17 |b 22 |c 10 |h e1635-e1646 | ||