Bisecting N-Acetylglucosamine Correlates with Phospho-Tau181 in Subjective Cognitive Decline but not in Control Cases.

Alzheimer’s disease N-glycosylation bisecting N-acetylglucosamine dementia mild cognitive impairment phospho-tau subjective cognitive decline total tau

Journal

Journal of Alzheimer's disease : JAD
ISSN: 1875-8908
Titre abrégé: J Alzheimers Dis
Pays: Netherlands
ID NLM: 9814863

Informations de publication

Date de publication:
07 Aug 2024
Historique:
medline: 9 8 2024
pubmed: 9 8 2024
entrez: 9 8 2024
Statut: aheadofprint

Résumé

The N-glycan structure bisecting N-acetylglucosamine (bisecting GlcNAc) is present on several N-glycans that are elevated in Alzheimer's disease (AD), and previous studies have shown that bisecting GlcNAc levels correlate with total tau and phospho-tau181 in cerebrospinal fluid at early stages of AD. A recent population-based study showed that bisecting GlcNAc correlates with total tau also in blood and that this correlation could predict conversion to dementia. In this study, we have further investigated how bisecting GlcNAc relates to total tau and phospho-tau 181 in cerebrospinal fluid samples from controls and cases with early cognitive deficits, stratified by amyloid/tau status and gender. Relative levels of bisecting GlcNAc in cerebrospinal fluid were measured by an enzyme-linked lectin assay in individuals with subjective cognitive decline, mild cognitive impairment and controls from the Norwegian Dementia Disease Initiation cohort. As in our previous study, the correlation between bisecting GlcNAc and total tau or phospho-tau181 was particularly strong in the subjective cognitive decline group. The correlation was observed in amyloid negative and tau negative as well as amyloid positive and tau positive individuals, both in females and in males. Interestingly, among the amyloid negative and tau negative individuals, the correlation was observed in individuals with subjective cognitive decline but not in the controls. Thus, bisecting GlcNAc could be a biomarker for early cognitive decline.

Sections du résumé

Background UNASSIGNED
The N-glycan structure bisecting N-acetylglucosamine (bisecting GlcNAc) is present on several N-glycans that are elevated in Alzheimer's disease (AD), and previous studies have shown that bisecting GlcNAc levels correlate with total tau and phospho-tau181 in cerebrospinal fluid at early stages of AD. A recent population-based study showed that bisecting GlcNAc correlates with total tau also in blood and that this correlation could predict conversion to dementia.
Objective UNASSIGNED
In this study, we have further investigated how bisecting GlcNAc relates to total tau and phospho-tau 181 in cerebrospinal fluid samples from controls and cases with early cognitive deficits, stratified by amyloid/tau status and gender.
Methods UNASSIGNED
Relative levels of bisecting GlcNAc in cerebrospinal fluid were measured by an enzyme-linked lectin assay in individuals with subjective cognitive decline, mild cognitive impairment and controls from the Norwegian Dementia Disease Initiation cohort.
Results UNASSIGNED
As in our previous study, the correlation between bisecting GlcNAc and total tau or phospho-tau181 was particularly strong in the subjective cognitive decline group. The correlation was observed in amyloid negative and tau negative as well as amyloid positive and tau positive individuals, both in females and in males. Interestingly, among the amyloid negative and tau negative individuals, the correlation was observed in individuals with subjective cognitive decline but not in the controls.
Conclusions UNASSIGNED
Thus, bisecting GlcNAc could be a biomarker for early cognitive decline.

Identifiants

pubmed: 39121127
pii: JAD240628
doi: 10.3233/JAD-240628
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Auteurs

Sofia Egebäck Arulf (S)

Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Karolinska Institutet, Solna, Sweden.

Robin Ziyue Zhou (R)

Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Karolinska Institutet, Solna, Sweden.

Bjørn-Eivind Kirsebom (BE)

Department of Neurology, University Hospital of North Norway, Troms-, Norway.
Department of Psychology, Faculty of Health Sciences, The Arctic University of Norway, Troms-, Norway.
Department of Neurology, Akershus University Hospital, L-renskog, Norway.
Institute of Clinical Medicine, Campus Ahus, University of Oslo, Oslo, Norway.

Alenka Jejcic (A)

Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Karolinska Institutet, Solna, Sweden.

Tormod Fladby (T)

Department of Neurology, Akershus University Hospital, L-renskog, Norway.
Institute of Clinical Medicine, Campus Ahus, University of Oslo, Oslo, Norway.

Bengt Winblad (B)

Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Karolinska Institutet, Solna, Sweden.
Theme Inflammation and Aging, Karolinska University hospital, Huddinge, Sweden.

Lars Tjernberg (L)

Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Karolinska Institutet, Solna, Sweden.

Sophia Schedin-Weiss (S)

Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Karolinska Institutet, Solna, Sweden.

Classifications MeSH