Psychiatry and clinical neurosciences · 2008
Prion disease causes less severe lesions in human hippocampus than other parts of brain.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Kaneko Minoru, Sugiyama Nobuhiro, Sasayama Daimei, Yamaoka Keiko, Miyakawa Tomohiro, Arima Kunimasa, Tsuchiya Kuniaki, Hasegawa Kazuko, Washizuka Shinsuke, Hanihara Tokiji, Amano Naoji, Yagishita Saburo
Аннотация
AIM: The hippocampus can be very sensitive to damage in the scrapie-infected mouse, a well-established animal model of prion diseases. Terminally ill scrapie-infected animals exhibit nearly complete loss of cornu ammonis (CA) 1 pyramidal neurons, but few studies have focused on the neuropathological lesions of the human hippocampus in autopsied brain tissue; in particular, few findings on differences in severity of pathology between the hippocampal and parahippocampal formations have been obtained. The aim of the present paper is to evaluate the human hippocampus of prion disease through neuropathological examination.
METHODS: A systemic, detailed neuropathological study throughout the subdivisions of the hippocampus was carried out in 23 autopsied cases of prion diseases. Prion protein immunohistochemistry was performed in serial brain sections to determine the topography of prion deposits.
RESULTS: Compared to lesions in other brain regions, hippocampal lesions were mild, despite numerous prion deposits. The distribution of prion deposits did not appear to be correlated with neuropathological changes. The present findings differed from the hippocampal pathology observed in scrapie-infected mice. In addition, differences in neuropathological severity were observed within the hippocampal formation.
CONCLUSION: The human hippocampus may be protected from the neurotoxic effects of prion deposits.
METHODS: A systemic, detailed neuropathological study throughout the subdivisions of the hippocampus was carried out in 23 autopsied cases of prion diseases. Prion protein immunohistochemistry was performed in serial brain sections to determine the topography of prion deposits.
RESULTS: Compared to lesions in other brain regions, hippocampal lesions were mild, despite numerous prion deposits. The distribution of prion deposits did not appear to be correlated with neuropathological changes. The present findings differed from the hippocampal pathology observed in scrapie-infected mice. In addition, differences in neuropathological severity were observed within the hippocampal formation.
CONCLUSION: The human hippocampus may be protected from the neurotoxic effects of prion deposits.