DOCOSAHEXAENOIC ACID (DHA): A NUTRITIONAL VIEW FOR THE PREVENTION OF ALZHEIMER'S DISEASE

Alzheimer's disease (AD) is a major public health problem in many countries of the world; however the specific cause of this disease is still unknown. Currently, a bulk of evidence supports the hypothesis that beta-amyloid peptide could be the cause of synaptic injuries and neuronal death observed at the initial stages of the disease. Patients with AD show lower levels of docosahexaenoic acid (DHA, C22: 6; omega-3) in plasma and brain tissue, as compared with age-matched controls. In addition, epidemiological studies indicate that a high intake of DMA may have protective properties against neurodegenerative diseases. These observations are supported by in vivo studies showing that diets rich in DHA reduce synaptic injuries and cognitive defects induced by the beta-amyloid peptide. Although the molecular basis of these neuroprotective effects are still unknown, a number of mechanisms have been proposed to explain this protection, such as: regulation in the expression of potentially protective genes, activation of anti-inflammatory pathways, and modulation of the functional properties of neuronal membranes along with changes in their structural characteristics and physical-chemical properties. The present work reviews and discusses the molecular basis of the hypothesis on the protective role of DHA in the prevention of AD. Alzheimer's disease (AD) is a major public health problem in many countries of the world; however the specific cause of this disease is still unknown. Currently, a bulk of evidence supports the hypothesis that beta-amyloid peptide could be the cause of synaptic injuries and neuronal death observed at the initial stages of the disease. Patients with AD show lower levels of docosahexaenoic acid (DHA, C22: 6; omega-3) in plasma and brain tissue, as compared with age-matched controls. In addition, epidemiological studies indicate that a high intake of DMA may have protective properties against neurodegenerative diseases. These observations are supported by in vivo studies showing that diets rich in DHA reduce synaptic injuries and cognitive defects induced by the beta-amyloid peptide. Although the molecular basis of these neuroprotective effects are still unknown, a number of mechanisms have been proposed to explain this protection, such as: regulation in the expression of potentially protective genes, activation of anti-inflammatory pathways, and modulation of the functional properties of neuronal membranes along with changes in their structural characteristics and physical-chemical properties. The present work reviews and discusses the molecular basis of the hypothesis on the protective role of DHA in the prevention of AD.