期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 22, 期 3, 页码 829-838出版社
IOS PRESS
DOI: 10.3233/JAD-2010-100663
关键词
A beta; cerebrospinal fluid; cortisol; frontal cortex; glucocorticoid receptor; mild cognitive impairment; mineralocorticoid receptor; Mini-Mental Status Examination
资金
- Stockholm County Council
- Karolinska Institute
- Riksbankens jubileum fond
- Loo och Hans Ostermans Stiftelse
- Gun och Bertil Stohnes Stiftelse
- Karolinska Institutets fund for geriatric research
- Stiftelsen Gamla Tjanarinnor
- Stiftelsen Dementia
- Stiftelsen Ragnhild och Einar Lundstroms Minne
- EC [MEST-CT-2005-019217]
- FIS [PI060200]
- Gobierno Navarra (Dpt. Salud)
- Foundation Ramon Areces
- Ministerio de Educacion y Ciencia (Spain)
The present work investigated the involvement of cortisol and its receptors, glucocorticoid receptor (GR) and mineralocorticoid receptor (MR), in Alzheimer's disease (AD). Cortisol was measured in cerebrospinal fluid (CSF) samples from controls, mild cognitive impairment (MCI), progressive MCI evolving to AD, and AD. CSF cortisol levels do not seem to have a prognostic value, as increases in cortisol levels were found only in AD patients. GR expression was decreased while MR expression was increased in the frontal cortex of AD. When considering degeneration (ratio to synaptophysin and the post-synaptic marker PSD95), GR expression was similar between controls and AD, suggesting that GR loss was due to synaptic degeneration in AD. Increases in cortisol levels and MR expression were associated to an apolipoprotein E4 genotype. Cognitive status was negatively associated to CSF cortisol. In apolipoprotein E4 carriers, MR but not GR expression, negatively correlated to Mini-Mental Status Examination score and positively correlated to frontal cortex amyloid-beta levels. It is concluded that there is a dysregulation of the hypothalamus-pituitary-adrenal axis in AD that seems to be consequence rather than cause of AD.
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