Understanding local Mediterranean diets: A multidisciplinary pharmacological and ethnobotanical approach

Epidemiological data indicate a beneficial effect of Mediterranean diets on human health, especially on the prevalence of cardiovascular disease. These observations are supported by recent intervention studies. However, very little is known about the current role of local Mediterranean food products, which are consumed on a less regular basis and their contribution to a healthy diet. The European consortium "Local Food-Nutraceuticals" collected 127 locally consumed wild or semi-wild plants in three Mediterranean countries, i.e. Greece, Italy, and Spain, in order to assess their ethnobotanical features as well as their biological activities. The project also includes a second line of research, the study of local conceptions about these food resources. All pharmacological assays were conducted with ethanolic extracts prepared from the dried plant material. The biological activities of the extracts were assessed with the following 12 different assays covering a broad range of mechanisms considered crucial in the pathology of chronic, aging-related diseases. Four antioxidant tests: DPPH scavenging, prevention of oxyhaemoglobin bleaching, prevention of lipid peroxidation (malondialdehyde formation), and protection from DNA damage (Comet assay); three enzyme inhibition tests: inhibition of xanthine oxidase, inhibition of myeloperoxidase-catalysed guaiacol oxidation as well as the inhibition of acetylcholine esterase; one test investigating the inhibition of cytokine-induced cell activation (including the extracts' potential cytotoxicity); one assay measuring the anti-proliferation potential; one test assessing the anti-diabetic activity (PPAR-gamma) as well as one assay investigating the extracts' effect on mood disorder-related biochemical parameters (hSERT). Furthermore, the polyphenol content of all extracts was determined using the Folin-Ciocalteaus method. The assays revealed diverse biological effects for the tested extracts ranging from no activity to almost complete inhibition/activation. Moreover, the experimental matrix led to the identification of a sub-set of extracts, i.e. Berberis vulgaris, Reichardia picroides, Scandix australis, Satureja montana, Thymus piperella, Lythrum salicaria and Vitis vinifera, showing high activity in a broad range of assays. In summary, the in vitro observed modulations and effects exerted by extracts derived from local food plants suggest that these plants may contribute to the observed better aging of rural Mediterranean populations. (c) 2005 Elsevier Ltd. All rights reserved

Mitochondrial dysfunction : common final pathway in brain aging and Alzheimer's disease : therapeutic aspects

As a fully differentiated organ, our brain is very sensitive to cumulative oxidative damage of proteins, lipids, and DNA occurring during normal aging because of its high energy metabolism and the relative low activity of antioxidative defense mechanisms. As a major consequence, perturbations of energy metabolism including mitochondrial dysfunction, alterations of signaling mechanisms and of gene expression culminate in functional deficits. With the increasing average life span of humans, age-related cognitive disorders such as Alzheimer's disease (AD) are a major health concern in our society. Age-related mitochondrial dysfunction underlies most neurodegenerative diseases, where it is potentiated by disease-specific factors. AD is characterized by two major histopathological hallmarks, initially intracellular and with the progression of the disease extracellular accumulation of oligomeric and fibrillar beta-amyloid peptides and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein. In this review, we focus on findings in AD animal and cell models indicating that these histopathological alterations induce functional deficits of the respiratory chain complexes and therefore consecutively result in mitochondrial dysfunction and oxidative stress. These parameters lead synergistically with the alterations of the brain aging process to typical signs of neurodegeneration in the later state of the disease, including synaptic dysfunction, loss of synapses and neurites, and finally neuronal loss. We suggest that mitochondrial protection and subsequent reduction of oxidative stress are important targets for prevention and long-term treatment of early stages of AD