Experimental dietary restriction (DR), vitamin E-deficiency and chronic ethanol administration were carried out on laboratory animals of different age to assess the role of nutrition on brain ageing. In DR mice, we measured the ultrastructural features of hippocampal synapses. The synaptic numeric density (Nv) was significantly increased, while the synaptic average size (S) was significantly reduced in old DR mice vs. ad libitum fed controls. These balanced changes resulted in a significant increase of the overall synaptic contact area/μm3 of tissue, i.e. surface density (Sv) in DR mice. Smaller contact zones were increased in old DR mice vs. ad libitum fed controls. Nv, S and Sv reliably report on synaptic plastic rearrangements, thus DR appears to be able to modulate positively synaptic structural dynamics in the ageing hippocampus. In adult-vitamin E-deficient rats and normally fed controls, we measured the intranuclear ionic content by means of X-ray microanalysis. K+ content resulted significantly increased in vitamin E-deficient rats, supporting the idea that the cellular membrane permeability of this ion is markedly impaired. In the cerebellar cortex and hippocampus of vitamin E-deficient animals we found that synaptic Nv and Sv were significantly decreased while S was increased: a pattern typical of the old animals. Computer-assisted morphometry of Purkinje cell mitochondria positive to succinic dehydrogenase (SDH) activity documented that in vitamin E-deficient animals the organelles' volume fraction as well as their average volume were significantly reduced. Vitamin E is a well known biological antioxidant able to quench the lipid peroxidation chain and to protect from free radical attacks, thus our data support that an increased oxidative stress occurs in adult vitamin E-deficient rats. Chronic alcohol intake in adult rats resulted in a significant increase of K+, a decrease of Na+ and no change in Cl-. Chronic ethanol intake in old rats vs. controls of the same age showed no change in K+ content, whereas both Na+ and Cl- decreased significantly. In adult ethanol-treated rats vs. their controls, synaptic Nv, S and Sv decreased significantly. In the old ethanol fed animals vs. age-matched controls, synaptic Nv and Sv decreased, while S was reduced at a not significant extent. These data confirm that neuronal membranes are markedly deteriorated by ethanol and that the excessive dietary intake of this alcohol affects their permeability and plasticity. Taken together, the findings of the three experimental dietary manipulations studied by us support the critical role of nutrition on the occurrence of age-related alterations in the brain. Namely, dietary components are significantly involved in various stages of the cellular antioxidant defense mechanisms and this appears to be of critical importance for the health status of the postmitotic nerve cells.
ASJC Scopus subject areas
- Clinical Neurology