In most areas of the world malnutrition in early life is directly or indirectly responsible of more deaths in children than other causes. Malnutrition is also a main concern in aged population. Nutritional deficiencies affect physical growth but also may produce irreversible mental and emotional changes. Many of these undesirable effects have been studied in animals [1]. Nutrition is of growing importance in degenerative diseases. Nilsson and coworkers have published that episodic memory performance i.e. the ability to recall events in time and place declines linearly with age. This decline in episodic memory began as early as at 20 years of age [2]. Thus, studies about nutrition influences in cognition should begin at early ages (20 years age or even less). Recent investigations in animals, on the physical and biochemical aging of the central nervous system, have provided helpful information to understand the effects of malnutrition. During maturation and growth, the amount of water in the brain gradually decreases, whereas the amount of cholesterol steadily increases [3, 4]. Maturation consists of a rapid increase in cells, as indicated by the increased concentrations phosphorus of DNA. Whereas growth parallels myelination and is represented by increased amounts of cholesterol [4,5]. Inadequate nutrition in calories and proteins, coinciding with the period in life in which the brain is growing most rapidly, may result in a smaller (than in controls) brain at maturity. Also, in a brain which matures biochemically and functionally at a slower rate [5]. In the adult rat starvation does not result in significant changes in brain weight or in damages to neural tissue. However, malnutrition associated -oxidative stress and -inflammation occur in neurons and astrocytes in elderly brains which may damage differently neural tissues in a differential fashion [6]. A biological mechanism which can be linked to nutrition and have been associated with aging includes oxidative stress [7], inflammation [8], homocysteine [9], advanced glycation end products [10] and the provision of fatty acids [11]. These mechanisms have in common that they reflect the nature of the existing diet or eventually respond to changes in what we eat. Changes from normal cognition to dementia, which affect in specific brain structures, usually take place slowly over decades. It is in this time-dependent scenario where general brain shrinkage, reduced cerebral blood impaired, glucose tolerance, or related patterns may prove to be useful endpoints [12].