Improved mitochondrial function in brain aging and Alzheimer disease - the new mechanism of action of the old metabolic enhancer piracetam

Kristina Leuner

doi:10.3389/fnins.2010.00044

Abstract

Piracetam, the prototype of the so-called nootropic drugs’ is used since many years in different countries to treat cognitive impairment in aging and dementia. Findings that piracetam enhances fluidity of brain mitochondrial membranes led to the hypothesis that piracetam might improve mitochondrial function, e.g., might enhance ATP synthesis. This assumption has recently been supported by a number of observations showing enhanced mitochondrial membrane potential, enhanced ATP production, and reduced sensitivity for apoptosis in a variety of cell and animal models for aging and Alzheimer disease. As a specific consequence, substantial evidence for elevated neuronal plasticity as a specific effect of piracetam has emerged. Taken together, this new findings can explain many of the therapeutic effects of piracetam on cognition in aging and dementia as well as different situations of brain dysfunctions.

Highlights

Piracetam, the prototype of the so-called “nootropic” drugs is used in many countries to treat cognitive impairment in aging, brain injuries, as well as dementia (Muller et al, 1999; Winblad, 2005)
Findings that piracetam enhances fluidity of brain mitochondrial membranes led to the hypothesis that piracetam might improve mitochondrial function, e.g., might enhance ATP synthesis.This assumption has recently been supported by a number of observations showing enhanced mitochondrial membrane potential, enhanced ATP production, and reduced sensitivity for apoptosis in a variety of cell and animal models for aging and Alzheimer disease
Piracetam, the prototype of the so-called “nootropic” drugs is used in many countries to treat cognitive impairment in aging, brain injuries, as well as dementia (Muller et al, 1999; Winblad, 2005)

Summary

Introduction

The prototype of the so-called “nootropic” drugs is used in many countries to treat cognitive impairment in aging, brain injuries, as well as dementia (Muller et al, 1999; Winblad, 2005). A major link between the mitochondrial defects of our brain accumulating during decades of aging and the specific Aß related toxicity in AD seems to be oxidative stress induced by Aß as well as Aß induced impairment of mitochondrial function, e.g., reduced activity of the complexes I and IV of the respiratory chain.

Results

Conclusion