Interplay between the APOE Genotype and Possible Plasma Biomarkers in Alzheimer's Disease
Jazyk angličtina Země Spojené arabské emiráty Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
29852871
DOI
10.2174/1567205015666180601090533
PII: CAR-EPUB-90848
Knihovny.cz E-zdroje
- Klíčová slova
- Alzheimer's disease, apolipoprotein E, cortisol, homocysteine, melatonin, prolactin.,
- MeSH
- Alzheimerova nemoc krev genetika MeSH
- apolipoproteiny E genetika MeSH
- biologické markery krev MeSH
- genotyp MeSH
- homocystein krev MeSH
- hydrokortison krev MeSH
- lidé středního věku MeSH
- lidé MeSH
- melatonin krev MeSH
- prolaktin krev MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- apolipoproteiny E MeSH
- biologické markery MeSH
- homocystein MeSH
- hydrokortison MeSH
- melatonin MeSH
- prolaktin MeSH
BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder with a complex pathogenesis and a common occurrence of comorbid diseases such as depression. It is accepted that the presence of the ε4 allele of the gene that encodes apolipoprotein E (APOE) is the strongest genetic risk factor for the development of sporadic AD. Melatonin, cortisol, homocysteine, and prolactin are presumed to be risk factors or biomarkers for stress- and age-related disorders. OBJECTIVE: The interplay between the APOE genotype and plasma biomarkers was examined in patients with AD presenting with or without depression to contribute to understanding the interdependence of various molecular mechanisms in the pathophysiology of AD. METHOD: The APOE genotype and morning plasma melatonin, cortisol, homocysteine, and prolactin concentrations were measured in 85 patients with AD and 44 elderly controls. RESULTS: A significant association between AD and the allele (ε4) or genotype (ε3/ε4 or ε4/ε4) frequencies of APOE was confirmed. Plasma homocysteine and cortisol levels were significantly increased in patients with AD compared to those in controls, independent of the presence of comorbid depressive symptoms or the severity of dementia. Significantly lower plasma melatonin concentration was found in patients with AD but not in controls, who were noncarriers of the APOE ε4 allele, regardless of the presence of depression or the severity of dementia in AD. CONCLUSION: Our findings indicate the existence of a little-known specific APOE-mediated mechanism that increases the plasma melatonin level in a subgroup of patients with AD who are carriers of the APOE ε4 allele.
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