Atıf İçin Kopyala
Akyol S., Ugurcu V., Cakmak O., Altuntas A., Yukselten Y., Akyol O., ...Daha Fazla
KLINIK PSIKOFARMAKOLOJI BULTENI-BULLETIN OF CLINICAL PSYCHOPHARMACOLOGY, cilt.24, sa.4, ss.323-332, 2014 (SCI-Expanded)
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Yayın Türü:
Makale / Tam Makale
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Cilt numarası:
24
Sayı:
4
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Basım Tarihi:
2014
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Doi Numarası:
10.5455/bcp.20140905124459
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Dergi Adı:
KLINIK PSIKOFARMAKOLOJI BULTENI-BULLETIN OF CLINICAL PSYCHOPHARMACOLOGY
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Derginin Tarandığı İndeksler:
Science Citation Index Expanded (SCI-EXPANDED), Scopus, TR DİZİN (ULAKBİM)
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Sayfa Sayıları:
ss.323-332
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Anahtar Kelimeler:
ADAMTS5, IL-33, NF kappa B, diabetes, hyperglycemia, Alzheimer's disease, matrix degradation, AMYLOID PRECURSOR PROTEIN, CENTRAL-NERVOUS-SYSTEM, NF-KAPPA-B, DEGRADING ENZYME, DIABETES-MELLITUS, BETA-PROTEIN, POSTNATAL-DEVELOPMENT, CONVERTING ENZYME, IN-VIVO, BRAIN
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Ankara Üniversitesi Adresli:
Evet
Özet
Objective: Alzheimer's disease (AD) is a progressive and irreversible central nervous system disease, which slowly destroys cognitive skills and memory, and eventually even the ability to handle the simplest tasks. The initiation and progression of AD is a poorly understood complex process. Here, we have investigated possible biological mechanisms that could be responsible for the increased risk for diminished brain function associated with diabetes in AD.