Alzheimer's disease and astrocytes
The destructive role of astrocyte activation in Alzheimer's disease has been confirmed
LifeSciencesToday based on materials from the University of Kentucky:
UK Team Inhibits Alzheimer's Biomarkers in Animal Model by Targeting AstrocytesA group of scientists from the University of Kentucky, led by Associate Professor of the Department of Molecular and Biochemical Pharmacology at the UK Medical College Christopher Norris, PhD, published an article for the first time evidently confirming the detrimental role of astrocyte activation in the development of Alzheimer's disease (Furman et al., Targeting Astrocytes Ameliorates Neurological Changes in a Mouse Model of Alzheimer's Disease).
In addition, The Sanders-Brown Center on Aging (The UK Sanders-Brown Center on Aging), of which Dr. Norris is a research associate, has received significant funds from the National Institutes of Health (National Institutes of Health) of the USA for the further development of this research area.
Astrocytes are widely distributed cells in the brain that are not related to nerve cells, performing the most important functions of providing a favorable environment for the functioning of nervous tissue. However, in neurodegenerative diseases such as Alzheimer's disease, obvious morphological and biochemical changes are observed in many astrocytes, often referred to by one general term "astrocyte activation". These changes appear to suppress the protective function of astrocytes and probably contribute to the development of neuroinflammation. The appearance of activated astrocytes in the very early stages of Alzheimer's disease has led scientists to believe that these cells may contribute to the emergence and/or maintenance of other pathological markers of this disease, including synaptic dysfunction and the formation of amyloid plaques.
Using genetic engineering, using an adeno-associated virus (AAV) containing an astrocyte-specific Gfa2 promoter as a vector, the researchers targeted the astrocytes of the hippocampus of mice with an Alzheimer's disease model (APP/PS1 line) and, thus, changed the degree of activation of these cells. AAV-Gfa2 vectors stimulated the expression of VIVIT, a peptide interfering with the calcineurin/NFAT (nuclear factor of activated T cells) signaling pathway responsible for biochemical cascades leading to astrocyte activation.
This genetic manipulation was carried out before the development of pronounced amyloid pathology in mice, and the condition of the animals was assessed after 10 months using several biomarkers of Alzheimer's disease. All this time, the mice received Gfa2-VIVIT.
The scientists concluded that the suppression of astrocyte activation leads, in turn, to the suppression of the activation of microglia (neuroinflammation intermediary cells), reduces the levels of toxic amyloid, positively affects synaptic plasticity and cognitive abilities of animals.
Thus, the study confirms the destructive role of astrocyte activation in Alzheimer's disease and the correctness of the concept of their therapeutic targeting. According to Dr. Norris and his colleagues, the findings lay the foundation for the development of treatments for patients suffering from Alzheimer's disease, or possibly other neurodegenerative diseases, the target of which will be astrocytes.
Portal "Eternal youth" http://vechnayamolodost.ru20.12.2012