People at risk for Alzheimer’s disease could benefit from a healthy diet, low in fats and sugars, as a preventive intervention. This was revealed by a group of researchers from Argentina, Mexico and Uruguay, who conducted an experimental study with laboratory animals.

Our results support the theory that an unhealthy diet accelerates the pathogenic mechanisms that trigger in the brain in early stages of Alzheimer’s, and it would function as the third negative factor for the development of the disease, after age and genetic predisposition,”said study director Dr. Laura Morelli, a researcher at the Argentinian National Scientific and Technical Research Council (CONICET).

A number of studies had already shown that cognitive impairment is more pronounced in Alzheimer’s patients with metabolic and vascular disorders. So the group of Latin American researchers decided to study biological mechanisms that would link those factors.

Based at the Laboratory of Amyloidosis and Neurodegeneration, which is led by Dr. Eduardo Castaño at the Leloir Institute (FIL), Morelli and her colleagues performed experiments with transgenic rodents recreating early forms of Alzheimer’s disease, provided by McGill University in Montreal, Canada. And they compared their evolution against control models.

As described in the journal Biochimica et Biophysica Acta-Molecular Basis of Disease, half of the animals in each group were fed from weaning a standard diet and the other half were fed a high fat and sugars diet, which is known as “western diet”. After six months, rodents underwent behavioral tests that evaluate memory and learning.

Scientists also carried out molecular studies of the brain, especially of the hippocampus, as this is the main area affected by the accumulation of beta-amyloid peptide protein in Alzheimer’s disease, and plays a fundamental role in memory processing.

According to Morelli, the western diet altered the “defense mechanisms” of the neurons in both groups of animals, but only affected learning and short-term memory in the group of animal models of Alzheimer’s disease.

We observed the decrease in expression of the Sirtuin 1 gene in the hippocampus, major regulator of energy metabolism, cell survival and neuroprotection,” said Morelli. “We also found that the ‘shutdown’ of the Sirtuin 1 gene inhibits two other genes that are very important: PGC-1α, which promotes mitochondrial functionality and antioxidant activity; and SOD2, which prevents the accumulation of reactive oxygen species within the mitochondria, thus silencing the pathways that protect the brain from situations that undermine its proper functioning.”

Our study reinforces the impact of an unhealthy diet on the beta-amyloid peptide brain’s metabolism, increasing its production and modifying it pathologically; and on neuronal resilience, thus diminishing the neurons’ ability of adapting to stressful situations,” she added.

The work supports a population-based dietary intervention as a relevant non-pharmacological strategy, at least in people aged 45-50 with genetic and vascular risk factors for Alzheimer’s disease,” said Morelli.

 

Source: Agencia ID