Alzheimer’s – clearing the plaques
Rostock – German researchers say overexpression of one of the 49 transport proteins that shuttle substances over the blood-brain barrier could be the key to treating Alzheimer’s disease. In mice, the group headed by Jens Pahnke from Rostock University has provided the proof-of-concept for their hypothesis that the onset of AD may be linked to a decrease in activity of the ABCC1 transporter (J Clin Invest., doi: 10.1172/JCI57867). In the brains of ABCC1-deficient transgenic mice, the Ab protein that forms the characteristic Alzheimer plaques accumulated 12- to 14-fold within 150 days compared to mice with the functional transporter. “We believe that clearance of Ab from the brain is the true problem with Alzheimer’s disease,” Pahnke said,“thus we looked for a way to accelerate it.” In screening for potential ABCC1 activators, Pahnke et al. found a highly-effective candidate in an FDA-approved drug against vomiting (Tiethylperazin). After one month of administration, it led to a drop of 75% in the Ab found in the brains of the mice, and improved their Alzheimer’s symptoms. Pahnke believes that the concept that the disease is due to deficient Ab transport over the blood-brain barrier is consistent with the fact that such transport requires a lot of energy, which is provided by mitochondria. In the course of ageing, mitochondrial activity is reduced. He now wants to test the hypothesis in clinical trials with pharma partners.