Tohoku University · Medicine
Professor Atsushi Takeda's research lab focuses on the neurobiological and molecular mechanisms underlying neurological and metabolic disorders, particularly Parkinson’s disease and oculocutaneous albinism. The lab investigates the link between brain glucose metabolism and clinical symptoms such as hyposmia in Parkinson’s disease using PET imaging and metabolic mapping. It also conducts molecular genetic analyses to identify disease-causing mutations, as demonstrated in their work on tyrosinase gene defects in tyrosinase-negative oculocutaneous albinism. The lab integrates clinical neuroscience with molecular genetics to uncover early biomarkers and genetic causes of neurodegenerative and pigmentation disorders.
Figures are computed from collected data and may differ slightly.
Hyposmia is one of the cardinal early symptoms of Parkinson disease (PD). Accumulating clinical and pathological evidence suggests that dysfunction of the olfactory-related cortices may be responsible for the impaired olfactory processing observed in PD; however, there are no clear data showing a direct association between altered brain metabolism and hyposmia in PD. In this study, we evaluated brain glucose metabolism and smell-identification ability in 69 Japanese patients with nondemented PD.
Tyrosinase-negative oculocutaneous albinism (OCA) is one of classical inborn errors of metabolism, characterized by a complete lack of melanin pigments in the eyes and skin. We have isolated and characterized the tyrosinase gene of one child (F. S.) affected with tyrosinase-negative OCA. Sequence analysis reveals a single-base mutation in the exon 1 (a G to A transition at nucleotide residue 312), causing the Arg (CGG) to Gln (CAG) substitution at position 59. This base change eliminates one Msp
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