Cerebral Ischemia and Alzheimer's Disease: The Expression of Amyloid-β and Apolipoprotein E in Human Hippocampus
| Autor: | Dandan Wang, Tao Liu, Ji-ping Qi, Yunhe Gu, He Wu, Yi Yang, Yan-xi Chen |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Adult
Male Apolipoprotein E Pathology medicine.medical_specialty Time Factors Ischemia Disease Stimulus (physiology) Hippocampus Brain Ischemia Pathogenesis Amyloid beta-Protein Precursor Apolipoproteins E Downregulation and upregulation Alzheimer Disease mental disorders medicine Humans Aged Vascular disease business.industry General Neuroscience Neurodegeneration General Medicine Middle Aged medicine.disease Psychiatry and Mental health Clinical Psychology nervous system Female Geriatrics and Gerontology business |
| Zdroj: | Journal of Alzheimer's Disease. 12:335-341 |
| ISSN: | 1875-8908 1387-2877 |
| DOI: | 10.3233/jad-2007-12406 |
| Popis: | Growing evidence suggests a synergistic and perhaps etiological relationship between vascular disease and Alzheimer's disease (AD), which is characterized by the progressive accumulation of amyloid-beta peptide (Abeta). Moreover, apolipoprotein E (ApoE) has also been shown to be associated with AD and cerebral ischemia. It seems that cerebral ischemia may play an important, both direct and indirect, role in the pathogenesis of AD. We investigated the expression and distribution of Abeta1-40, beta1-42 and ApoE in human hippocampus after cerebral ischemia in this study to determine the role of cerebral ischemia in Alzheimer's disease. Our study has demonstrated that the accumulation of both Abeta1-40 and beta1-42 were increased dramatically and consistently after cerebral ischemia. Neuronal ApoE immunoreactivity was also significantly increased in all ischemic groups compared with controls. The most likely stimulus for the increased Abeta1-40, Abeta1-42 and ApoE immunoreactivity in the CA1 and CA3 neurons is the ischemic conditions, and their upregulation, in turn, may partly explain the contribution of cerebral ischemia to the pathogenesis of AD. Therefore our observations provide a basis for establishing therapeutic strategies aimed at preventing ischemic insults and subsequent neurodegeneration in AD. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|