Cel Research in recent years has started to provide an alternative view to Alzheimer's etiology emphasizing the role of other factors such as inflammation and brain vascular alterations in the development of Alzheimer. Of major interest is the link between AD and hypertension, another global epidemic affecting millions of people worldwide. Hypertension resultsin increased stiffness of the brain vasculature leading, among others, to chronic cerebral hypoperfusion. Little is known about the short and long-term consequences of such hypoperfusion on neuronal dynamics. Hypoperfusion alters the function of the blood brain barrier; a cellular ensemble that actively keeps at bay pathogens and alike from entering the brain parenchyma. Amyloid and its products are under strict control across this barrier. Hence, damage to the barrier results in their accumulation in the brain parenchyma, which likely contributes to neuronal dysfunction and dementia. This recently recognized tight association between AD and hypertension opens new venues for both basic and translational researchwith the promise to better understand and likely treat these two maladies together. Dziedzina nauki medical and health sciencesbasic medicineneurologydementiaalzheimer Program(-y) FP7-PEOPLE - Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) Temat(-y) FP7-PEOPLE-2013-CIG - Marie-Curie Action: "Career Integration Grants" Zaproszenie do składania wniosków FP7-PEOPLE-2013-CIG Zobacz inne projekty w ramach tego zaproszenia System finansowania MC-CIG - Support for training and career development of researcher (CIG) Koordynator TEL AVIV UNIVERSITY Wkład UE € 100 000,00 Adres RAMAT AVIV 69978 Tel Aviv Izrael Zobacz na mapie Rodzaj działalności Higher or Secondary Education Establishments Kontakt administracyjny Lea Pais (Ms.) Linki Kontakt z organizacją Opens in new window Strona internetowa Opens in new window Koszt całkowity Brak danych
