Iron and Ferritin Deficiencies in the Cerebral Cortex of Senescence-accelerated Mouse Prone 10

• Published in: Biomedical Research on Trace Elements Vol. 23; no. 4; pp. 230 - 235
• Main Authors: Miyajima, Miki, Numata, Takuya, Minoshima, Moemi, Tanaka, Masato, Nishimura, Ryo, Hishioka, Naoko, Hosokawa, Toshiyuki, Kurasaki, Masaaki, Saito, Takeshi
• Format: Journal Article
• Language: English; Japanese
• Published: Osaka Japan Society for Biomedical Research on Trace Elements 31.12.2012; Japan Science and Technology Agency
• Subjects: brain; catecholamines; Cognitive ability; ferritin; Iron; SAMP10; tyrosine hydroxylase
• ISSN: 0916-717X; 1880-1404
• DOI: 10.11299/brte.23.230

Previous studies have shown that iron (Fe) is essential for tyrosine hydroxylase (TH) activity and is a risk -factor for cognitive decline and brain atrophy. The senescence-accelerated mouse prone 10 (SAMP10) stain exhibits a decline of catecholamines, brain atrophy, and behavioral deterioration, such as dysfunctions in learning and memory, with advancing age. The purpose of this study was to elucidate the contribution of iron to catecholamine metabolism in the brains of SAMP10 mice. Iron concentration was determined using an inductively coupled plasma mass spectrometer. Expression of the metal binding proteins ferritin, divalent metal transporter-1 (DMT1), and hepcidin was determined by western blot analysis. The present study demonstrated that iron and ferritin levels in SAMP10 mice were significantly lower than that in control animals. DMT1 and hepcidin levels, however, did not differ significantly between SAMP10 and control mice. Our previous study showed that the decline in dopamine (DA) and norepinephrine (NE) concentrations in the cerebral cortex of SAMP10 mice is caused by downregulation of TH activity. Given that Fe is necessary for TH activity, our results suggest that a decrease in iron causes the decline of TH activity in the cerebral cortex of SAMP10 mice.