期刊
NEUROLOGY
卷 90, 期 19, 页码 E1682-E1691出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0000000000005476
关键词
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资金
- Swedish Research Council [2012-5041, 2013-8717, 2015-02830]
- Swedish Research Council for Health, Working Life and Welfare [2013-1202, AGECAP 2013-2300, 2013-2496, 20130475]
- Swedish Alzheimerfoundation
- Hjarnfonden
- Stena Foundation
- Sahlgrenska University Hospital (ALF)
- Torsten Soderbergs Stiftelse at the Royal Swedish Academy of Sciences
- Knut and Alice Wallenberg Foundation
- Emil and Maria Palm Foundation
- Alma och Anna Ylen's Foundation
- Konung Gustaf V:s och Drottning Victorias Frimurarestiftelse
- Eivind och Elsa K:son Sylvans stiftelse
- Stiftelsen Soderstrom-Konigska Sjukhemmet
- Stiftelsen for Gamla Tjanarinnor
- Handlanden Hjalmar Svenssons Forskningsfond
- Stiftelsen Demensfonden
- Stiftelsen Wilhelm and Martina Lundgrens Vetenskapsfond
- Stiftelsen Professor Bror Gadelius' Minnesfond
- Goteborg Medical Services and Social Services Administrations
- Fredrik and Rosa von Malborgs Foundation for Brain Research
- Swedish Research Council [2015-02830] Funding Source: Swedish Research Council
Objective To determine the prevalence of preclinical Alzheimer disease (AD) according to current classification systems by examining CSF from a representative general population sample of 70-year-olds from Gothenburg, Sweden. Method The sample was derived from the population-based H70 Gothenburg Birth Cohort Studies in Gothenburg, Sweden. The participants (n = 322, age 70 years) underwent comprehensive neuropsychiatric, cognitive, and somatic examinations. CSF levels of beta-amyloid (A beta)(42), A beta(40), total tau, and phosphorylated tau were measured. Preclinical AD was classified according to criteria of the A/T/N system, Dubois 2016, National Institute on Aging-Alzheimer's Association (NIA-AA) criteria, and International Working Group-2 (IWG-2) criteria. Individuals with Clinical Dementia Rating score > 0 were excluded, leaving 259 cognitively unimpaired individuals. Results The prevalence of amyloid pathology was 22.8%, of total tau pathology was 33.2%, and of phosphorylated tau pathology was 6.9%. With the A/T/N system, the prevalence of A+/T-/N- was 13.1%, A+/T-/N+ was 7.3%, A+/T+/N+ was 2.3%, A-/T-/N+ was 18.9%, and A-/T+/N+ was 4.6%. When the Dubois criteria were applied, the prevalence of asymptomatic at risk for AD was 36.7% and of preclinical AD was 9.7%. With the NIA-AA criteria, the prevalence of stage 1 was 13.1% and stage 2 was 9.7%. With the IWG-2 criteria, the prevalence of asymptomatic at risk for AD was 9.7%. The APOE epsilon 4 allele was associated with several of the categories. Men more often had total tau pathology, A+/T-/N+, preclinical AD according to Dubois 2016, asymptomatic at risk for AD according to the IWG-2 criteria, and NIA-AA stage 2. Conclusion The prevalence of pathologic AD markers was very common (46%) in a representative population sample of 70-year-olds. The clinical implications of these findings need to be scrutinized further in longitudinal studies.
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