Abstract
Hyperhomocysteinemia (hHcy) is regarded as an independent and strong risk factor for cerebrovascular diseases, stroke, and dementias. The hippocampus has a crucial role in spatial navigation and memory processes and is being constantly studied for neurodegenerative disorders. We used a moderate methionine (Met) diet at a dose of 2 g/kg of animal weight/day in duration of four weeks to induce mild hHcy in adult male Wistar rats. A novel approach has been used to explore the hippocampal metabolic changes using proton magnetic resonance spectroscopy (1H MRS), involving a 7T MR scanner in combination with histochemical and immunofluorescence analysis. We found alterations in the metabolic profile, as well as remarkable histo-morphological changes such as an increase of hippocampal volume, alterations in number and morphology of astrocytes, neurons, and their processes in the selective vulnerable brain area of animals treated with a Met-enriched diet. Results of both methodologies suggest that the mild hHcy induced by Met-enriched diet alters volume, histo-morphological pattern, and metabolic profile of hippocampal brain area, which might eventually endorse the neurodegenerative processes.
Highlights
Several nutritional factors can influence the risk of development of neurodegenerative diseases and their rate of progression
We measured total N-Acetyl Aspartate, myo-Inositol, total choline and total creatine containing compounds which were expressed as following ratios: tNAA/tCr, mIns/tNAA, mlns/tCr, tCho/tNAA and tCho/tCr
Quantification of 1H MRS in the hippocampus of animals showed tNAA to tCr, mIns/tNAA and mlns/tCr ratios in Met-enriched diet group (MDG) group compared to the control
Summary
Several nutritional factors can influence the risk of development of neurodegenerative diseases and their rate of progression. Its elevated level in plasma, hyperhomocysteinemia (hHcy), is one of the known risk factors for cardioand cerebrovascular disorders. Development of the neurodegenerative disorders, such as progressive atherosclerosis and acute ischemic stroke, cognitive impairment, dementia, or Alzheimer’s disease (AD), is associated with hHcy [3,4,6], but the exact mechanism of its involvement in affecting neuronal tissue is not yet elucidated. S-adenosyl homocysteine (SAH), an intermediate of metabolic conversion of Hcy, was shown to be a metabolic sensor controlling methylation-regulated signalling within the Met-Hcy cycle. As a consequence, it potentially initiates the DNA and protein hypomethylation with an impact on diverse tissue disturbances, including neuronal cells [9]. The selective cytosolic and nuclear Hcy clearance is essential for cellular genetic protection
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