Does an integrative genome-wide transcriptome reveal that candesartan is neuroprotective and a candidate therapeutic for Alzheimer 's disease?
Our data may be interpreted as evidence of direct candesartan neuroprotection beyond its effects on blood pressure, revealing common and novel disease mechanisms that may underlie the in vitro gene alterations reported here and glutamate-induced cell injury in Alzheimer's disease. Our observations provide novel evidence for candesartan neuroprotection through early molecular mechanisms of injury in Alzheimer's disease, supporting testing this compound in controlled clinical studies in the early stages of the illness.
TLR4 activation in BE results in a strong increase in COX-2 and may contribute to malignant transformation.