4.5 Article

Reduced Cerebrospinal Fluid Concentration of Apolipoprotein A-I in Patients with Alzheimer's Disease

期刊

JOURNAL OF ALZHEIMERS DISEASE
卷 59, 期 3, 页码 1017-1026

出版社

IOS PRESS
DOI: 10.3233/JAD-170226

关键词

Alzheimer's disease; apolipoprotein A-I; apolipoprotein E; cerebrospinal fluid; lipids; other dementia

资金

  1. Swedish Research Council [523-2007-7111, 14003, 2013-2546, 521-20132572]
  2. European Research Council [681712]
  3. ALF/LUA research grant in Gothenburg [ALFGBG-438631, ALFGBG-139671, ALFGBG-441051, ALFGBG-73040]
  4. Lundberg Foundation
  5. Torsten and Ragnar Soderberg's Foundation
  6. Swedish Brain foundation
  7. Knut and Alice Wallenberg Foundation
  8. Lundbeck Foundation
  9. Sahlgrenska University Hospital
  10. Sahlgrenska Academy
  11. Stiftelsen Psykiatriska Forskningsfonden
  12. Stiftelsen Gamla Tjanarinnor
  13. Uppsala Universitets Medicinska Fakultet stiftelse for psykiatrisk och neurologisk forskning
  14. Alzheimer Foundation, Sweden
  15. Dementia Association, Sweden
  16. Frimurarestiftelsen

向作者/读者索取更多资源

Background: Apolipoprotein E (ApoE) has been extensively studied in Alzheimer's disease (AD), but little is known of apolipoprotein A-I (ApoA-I) in cerebrospinal fluid (CSF). Objective: Plasma lipids as well as ApoA-I and ApoE in plasma and CSF were determined and related to Mini-Mental State Examination (MMSE) score, APOE genotype, and CSF AD biomarkers. Methods: Consecutive patients with AD (n = 29), stable mild cognitive impairment (n = 13), other dementias (n = 14), and healthy controls (n = 18) were included at a single center. Results: AD patients had higher plasma triglycerides and lower CSF ApoA-I concentration than controls (both p < 0.05). CSF ApoE concentration was reduced in other dementias (p < 0.01). In AD as well as other dementias, the ratios between CSF and plasma concentrations of both ApoA-I and ApoE were lower than those in the controls. ApoA-I and ApoE in plasma and CSF were not influenced by APOE epsilon 4 allele distribution. In the total study population (n = 74), CSF ApoA-I correlated positively with MMSE score (r = 0.26, p < 0.05) and negatively with CSF P-tau (r = -0.25, p < 0.05). CSF ApoE correlated positively with CSF concentrations of T-tau and P-tau in the total study population and in AD patients. Conclusion: CSF ApoA-I was reduced in AD patients and associated with measures of cognitive function and AD disease status. The mechanisms underlying the decreased CSF: plasma ratios of ApoA-I and ApoE in AD and other dementias need to be explored in further studies.

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