**3. Conclusions**

Fibrates act as synthetic ligands for PPARα and are commonly used to treat hypertriglyceridemia and to prevent coronary heart disease. PPARα is also involved in the anti-inflammatory response and in improvement of mitochondrial function. Fibrate therapy reduces the incidence and delays the onset of type II diabetes and seems to improve insulin sensibility in humans (Goldenberg et al., 2008). A recent clinical study suggests that in hypertriglyceridemic individuals, bezafibrate increase the production of ketone bodies, the alternative energy source for the brain (Tremblay-Mercier et al., 2010). Thus, by reducing triglycerides, enhancing glucose availability, providing alternative brain fuel and improving cardiovascular profile, PPARα agonist could have relevant impact on the maintenance of a good cognitive health later in life (figure 8). Fibrate therapy may have potential as pharmacological agents aiming to reduce the risk of AD and future research are needed to determine if secondary prevention with fibrate therapy is able to delay the apparition of cognitive decline.

Fig. 8. Summary diagram on the PPARα agonist's action on modifiable risk factors for cognitive decline.
