Variability of protein and lipid composition of human subtantia nigra in aging: Fourier transform infrared microspectroscopy study

There is growing evidence that a variety of biochemical processes that underlie the most frequent neurodegenerative diseases may have much in common with those connected with natural aging. It was shown that they involve, among others, lipid peroxidation and/or generation of insoluble in water protein deposits (i.e. alpha-synuclein and/or beta amyloid). Therefore, it is likely that the analysis of changes in both lipid and protein composition may be interesting in the light of any potential pathologies occurring within the dopaminergic system during physiological aging. Thereby, this paper presents a methodology for the analysis of age-related changes in a lipid and protein composition within human subtantia nigra tissue by means of Fourier transform infrared microspectroscopy (FTIRM). Particularly, the changes in the lipid saturation, unsaturation as well as in the protein secondary structure were examined. The studies were carried out on samples from 35 individuals who died without any signs of neurologic dysfunctions. Our results show that the level of lipid saturation increases inside the subtantia nigra tissue with age, though the total content of lipid decreases with age of individuals. Moreover, the statistically significant decrease in the protein content within neuron bodies was observed. Interestingly, it is presented that the content of the anti-parallel beta sheets for neuron bodies decreases from seventh to eighth decades of life and subsequently markedly increases from eighth to ninth decades of life, whilst, as regards extraneuronal spaces, the opposite trends are reported i.e. increase from the seventh to eighth decades, and subsequent decrease in the ninth decade of life. These observations, though preliminary, shed the light on a putative contribution of various pathological lipid- and protein-related processes underlying senescence, suggesting a "biochemical link" between the aetiology of the most common neurodegenerative diseases and physiological aging.