Comparing high and low amyloid producers ...
Document type :
Article dans une revue scientifique: Article original
PMID :
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Title :
Comparing high and low amyloid producers in Alzheimer's disease: An in-depth analysis
Author(s) :
Leroy, Mélanie [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Excellence Laboratory LabEx DISTALZ
Aziz, Anne Laure [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Schraen, Susanna [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Excellence Laboratory LabEx DISTALZ
Deramecourt, Vincent [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Skrobala, Emilie [Auteur]
Excellence Laboratory LabEx DISTALZ
Lecerf, Simon [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Pasquier, Florence [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Excellence Laboratory LabEx DISTALZ
Huin, Vincent [Auteur]
Excellence Laboratory LabEx DISTALZ
Lille Neurosciences & Cognition (LilNCog) - U 1172
Bertoux, Maxime [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Excellence Laboratory LabEx DISTALZ
Lebouvier, Thibaud [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Excellence Laboratory LabEx DISTALZ
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Excellence Laboratory LabEx DISTALZ
Aziz, Anne Laure [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Schraen, Susanna [Auteur]

Lille Neurosciences & Cognition - U 1172 [LilNCog]
Excellence Laboratory LabEx DISTALZ
Deramecourt, Vincent [Auteur]

Lille Neurosciences & Cognition - U 1172 [LilNCog]
Skrobala, Emilie [Auteur]
Excellence Laboratory LabEx DISTALZ
Lecerf, Simon [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Pasquier, Florence [Auteur]

Lille Neurosciences & Cognition - U 1172 [LilNCog]
Excellence Laboratory LabEx DISTALZ
Huin, Vincent [Auteur]

Excellence Laboratory LabEx DISTALZ
Lille Neurosciences & Cognition (LilNCog) - U 1172
Bertoux, Maxime [Auteur]

Lille Neurosciences & Cognition - U 1172 [LilNCog]
Excellence Laboratory LabEx DISTALZ
Lebouvier, Thibaud [Auteur]

Lille Neurosciences & Cognition - U 1172 [LilNCog]
Excellence Laboratory LabEx DISTALZ
Journal title :
Revue Neurologique
Abbreviated title :
Rev Neurol (Paris)
Publisher :
Elsevier
Publication date :
2025-03-07
ISSN :
0035-3787
English keyword(s) :
Alzheimer's disease
Cerebrospinal fluid biomarkers
Aβ42/40 ratio
A/T/N
Cerebrospinal fluid biomarkers
Aβ42/40 ratio
A/T/N
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [en]
Background
The cerebrospinal fluid (CSF) Aβ42/40 ratio has proven to be a more reliable biomarker for amyloid pathology than CSF Aβ42 in Alzheimer's disease (AD), helping to correctly classify patients with positive tau ...
Show more >Background The cerebrospinal fluid (CSF) Aβ42/40 ratio has proven to be a more reliable biomarker for amyloid pathology than CSF Aβ42 in Alzheimer's disease (AD), helping to correctly classify patients with positive tau biomarkers (T+) that would otherwise have remained outside of the AD continuum. It was shown that the Aβ42/40 ratio better captures a relative decrease of Aβ42 in patients with high CSF Aβ. However, whether patients with high-amyloid (HiA) AD, in whom A+ is defined by the Aβ42/40 ratio, exactly compare with their low-amyloid (LoA) counterparts, in whom A+ is defined by Aβ42 solely, deserves further analysis. Methods We retrospectively included patients with A+T+ AD and evidence of cognitive and neurodegenerative changes (N+). LoA patients were operationally defined as patients with T+N+ and low CSF Aβ42, while HiA patients were defined as patients with T+N+ and normal CSF Aβ42 but abnormal Aβ42/40 ratio. Tau CSF biomarkers, neuropsychological profile, rates of cognitive decline, structural and metabolic imaging, ApoE genotype and brain neuropathology were compared between the HiA and LoA groups. Results At the time of the lumbar puncture, LoA patients were significantly younger than the HiA patients (68.9 ± 8.7 years vs. 71.8 ± 9.4; P = 0.0015) and had a lower Mini-Mental Status Examination (MMSE) (18.7 ± 6.4 vs. 20.7 ± 6.2; P = 0.0005). There was no difference in the neuropsychological profile nor in the annual rates of cognitive decline between the two groups with early AD. No differences were retrieved between groups on CSF Tau and P-Tau biomarkers, atrophy and brain metabolism, distribution of the APOE4 allele and APOE4/E4 genotype, and neuropathology. Conclusions Overall, our study supports the surrogate use of the Aβ42/40 ratio as an equivalent to Aβ42 to define AD. We showed that HiA CSF profiles were not associated with differences in cognition, brain structures and metabolism, APOE genotype tau CSF biomarkers or the rates of cognitive decline, but may be the associated with later-onset and early-stage AD.Show less >
Show more >Background The cerebrospinal fluid (CSF) Aβ42/40 ratio has proven to be a more reliable biomarker for amyloid pathology than CSF Aβ42 in Alzheimer's disease (AD), helping to correctly classify patients with positive tau biomarkers (T+) that would otherwise have remained outside of the AD continuum. It was shown that the Aβ42/40 ratio better captures a relative decrease of Aβ42 in patients with high CSF Aβ. However, whether patients with high-amyloid (HiA) AD, in whom A+ is defined by the Aβ42/40 ratio, exactly compare with their low-amyloid (LoA) counterparts, in whom A+ is defined by Aβ42 solely, deserves further analysis. Methods We retrospectively included patients with A+T+ AD and evidence of cognitive and neurodegenerative changes (N+). LoA patients were operationally defined as patients with T+N+ and low CSF Aβ42, while HiA patients were defined as patients with T+N+ and normal CSF Aβ42 but abnormal Aβ42/40 ratio. Tau CSF biomarkers, neuropsychological profile, rates of cognitive decline, structural and metabolic imaging, ApoE genotype and brain neuropathology were compared between the HiA and LoA groups. Results At the time of the lumbar puncture, LoA patients were significantly younger than the HiA patients (68.9 ± 8.7 years vs. 71.8 ± 9.4; P = 0.0015) and had a lower Mini-Mental Status Examination (MMSE) (18.7 ± 6.4 vs. 20.7 ± 6.2; P = 0.0005). There was no difference in the neuropsychological profile nor in the annual rates of cognitive decline between the two groups with early AD. No differences were retrieved between groups on CSF Tau and P-Tau biomarkers, atrophy and brain metabolism, distribution of the APOE4 allele and APOE4/E4 genotype, and neuropathology. Conclusions Overall, our study supports the surrogate use of the Aβ42/40 ratio as an equivalent to Aβ42 to define AD. We showed that HiA CSF profiles were not associated with differences in cognition, brain structures and metabolism, APOE genotype tau CSF biomarkers or the rates of cognitive decline, but may be the associated with later-onset and early-stage AD.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
European Project :
Administrative institution(s) :
Université de Lille
Inserm
CHU Lille
Inserm
CHU Lille
Collections :
Submission date :
2025-03-25T22:05:24Z
2025-04-08T11:05:37Z
2025-04-08T11:05:37Z
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