Response to Alzheimer’s research paper

Correspondence: H Mina Tait Group X10, Western Bank, Sheffield, S10 2TN, UK Tel +44 011 4222 0000 Fax +44 011 4276 5413 Email [email protected] Dear editor Zhang et al have recently published an interesting article in Clinical Interventions in Aging entitled “Atorvastatin attenuates the production of IL-1β, IL-6, and TNF-α in the hippocampus of an amyloid β1-42-induced rat model of Alzheimer’s disease”. The conclusion that “IL-1β, IL-6, and TNF-α were significantly decreased in the atorvastatin-treated AD group than that in the AD group” is not justified by the data presented in Figures 1, 2, and 3. Given that the AD group and the atorvastatintreated AD group showed no significant difference in numbers of cells positive for interleukin-1β, interleukin-6, or tumor necrosis factor-α, and in some cases there may be a trend towards an increase in positive cells in the atorvastatin-treated AD group, it is hard to see how they came to this conclusion. In their introduction, Li et al state that “Cholesterol-lowering agents, particularly 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (also known as statins), have been reported to be capable of increasing the ratio of alpha to beta secretase activity and then increasing the concentrations of extracellular Aβ.” The conventional wisdom, supported by the references that they cite (eg, Buxbaum et al), is that changing the ratio in this way is likely to lead to a decrease, not an increase, in extracellular Aβ. I would very much like to hear the authors’ and your views on these issues.