Tohoku University · Medicine
Professor Kentaro Tanemura's research lab focuses on the neurotoxicological and developmental impacts of environmental chemicals and genetic mutations on the central nervous system and reproductive health. The lab investigates mechanisms underlying neurodegeneration, particularly tau pathology and amyloid precursor protein processing in Alzheimer’s disease models, as well as the long-term neurological consequences of early-life exposure to neuroactive chemicals such as domoic acid, bisphenols, and pyrethroids. A key research direction involves understanding how low-dose, chronic exposure to environmental toxins during critical neurodevelopmental windows leads to persistent cognitive and behavioral deficits in adulthood. The lab also examines age-related morphological changes in reproductive tissues, particularly in the testis, to assess the effects of aging and chemical exposure on fertility.
Figures are computed from collected data and may differ slightly.
Formation of neurofibrillary tangles (NFTs) is a common neuropathological feature found in several neurodegenerative diseases, including Alzheimer's disease. We have developed a transgenic (Tg) mouse expressing mutant human tau (V337M), derived from frontotemporal dementia parkinsonism-17. V337M Tg mice revealed tau aggregations in the hippocampus, which fulfills the histological criteria for NFTs in human neurodegenerative diseases. Concurrent with the accumulation of RNA and phosphorylated tau
Mutations in the presenilin 1 (PS1) gene are responsible for the early onset of familial Alzheimer disease (FAD). Accumulating evidence shows that PS1 is involved in gamma-secretase activity and that FAD-associated mutations of PS1 commonly accelerate Abeta(1-42) production, which causes Alzheimer disease (AD). Recent studies suggest, however, that PS1 is involved not only in Abeta production but also in other processes that lead to neurodegeneration. To better understand the causes of neurodege
To demonstrate induction of delayed central nervous toxicity by disturbing neuronal activities in the developing brain, we administered a single intraperitoneal dose of domoic acid (DA; 1 mg/kg), a potent glutamate receptor agonist, to pregnant female mice at the gestational day of 11.5, 14.5 or 17.5. The dams had recovered from acute symptoms within 24 hr, followed by normal delivery, feeding and weaning. All male offspring mice after weaning were apparently normal in response to handlers durin
Age-related morphological changes in the testis of the BDF1 mouse were studied by light and transmission electron microscopy. No apparent changes were detected until 12 months of age. After 18 months of age, vacuoles firstly appeared in the seminiferous epithelium. These vacuoles were gradually increased in number and showed a tendency to cluster with each other in accordance with age. While, germ cells were decreased in number. The sloughing of germ cells caused a thin seminiferous epithelium.
Bisphenol AF (BPAF), a homolog of bisphenol A (BPA), is a widely used environmental chemical that has adverse effects on reproduction. The aim of this study was to analyse the effects of BPA and BPAF exposure on oocyte maturation in vitro. Oocytes were cultured in the presence of BPA or BPAF (2, 20, 50 or 100 μg/ml) for 18 h. At concentrations of 50 and 100 μg/ml, BPA and BPAF inhibited oocyte maturation, with BPAF treatment causing a sharp decrease in the number of oocytes reaching maturity. Oo
Permethrin, a pyrethroid chemical, is widely used as a pesticide because of its rapid insecticidal activity. Although permethrin is considered to exert very low toxicity in mammals, the effects of early, low-level, chronic exposure on the adult central nervous system are unclear. In this study, we investigated the effects of low-level, chronic permethrin exposure in early life on the brain functions of adult mice, using environmentally relevant concentrations. We exposed mice to the acceptable d
Tau is one of the microtubule-associated proteins and a major component of paired helical filaments, a hallmark of Alzheimer's disease. Its expression has also been indicated in the testis. However, its function and modification in the testis have not been established. Here, we analyzed the dynamics of phosphorylation patterns during spermatogenesis. The expression of Tau protein and its phosphorylation were shown in the mouse testis. Immunohistochemistry revealed that the phosphorylation was st
<i>Axdnd1</i> is essential for spermatogenesis in the mouse testes. These findings improve our understanding of spermiogenesis and related defects. According to a recent report, deleterious heterozygous mutations in AXDND1 were found in non-obstructive azoospermia (NOA) patients. Therefore, <i>Axdnd1</i> KO mice could be used as a model system for NOA, which will greatly contribute to future NOA treatment studies.
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