||Chang Shen, Hiroyuki Honda, Satoshi O Suzuki, Norihisa Maeda, Masahiro Shijo, Hideomi Hamasaki, Naokazu Sasagasako, Naoki Fujii, Toru Iwaki, Dynactin is involved in Lewy body pathology, Neuropathology, https://www.hakatarou.jp/top.html, 2018.11.
||Norihisa Maeda, Hiroyuki Honda, Satoshi O Suzuki, Naoki Fujii, Jun-ichi Kira, Toru Iwaki, Mitochondrial dysfunction and altered ribostasis in hippocampal neurons with cytoplasmic inclusions of multiple system atrophy, Neuropathology, 2018.05.
||Hiroyuki Honda, Naokazu Sasagasako, Chang Shen, Masahiro Shijo, Hideomi Hamasaki, Satoshi O. Suzuki, Yoshio Tsuboi, Naoki Fujii, Toru Iwaki, DCTN1 F52L mutation case of Perry syndrome with progressive supra nuclear palsy-like tauopathy, Parkinsonism and Related Disorders, 2018.03.
||Hiroyuki Honda, Kensuke Sasaki, Hiroshi Takashima, Daisuke Mori, Sachiko Koyama, Satoshi O Suzuki, Toru Iwaki, Different Complicated Brain Pathologies in Monozygotic Twins with Gerstmann-Sträussler-Scheinker Disease, Journal of Neuropathology & Experimental Neurology, in press, 2017.07.
||Yu-Tzu Wu, Alexa S. Beiser, Monique M. B. Breteler, Hiroyuki Honda, Carol Brayne, The changing prevalence and incidence of dementia over time current evidence, Nature Reviews Neurology, 10.1038/nrneurol, 13, 6, 327-339, 2017.06, Dementia is an increasing focus for policymakers, civil organizations and multidisciplinary researchers. The most recent descriptive epidemiological research into dementia is enabling investigation into how the prevalence and incidence are changing over time. To establish clear trends, such comparisons need to be founded on population-based studies that use similar diagnostic and research methods consistently over time. This narrative Review synthesizes the findings from 14 studies that investigated trends in dementia prevalence (nine studies) and incidence (five studies) from Sweden, Spain, the UK, the Netherlands, France, the USA, Japan and Nigeria. Besides the Japanese study, these studies indicate stable or declining prevalence and incidence of dementia, and some provide evidence of sex-specific changes. No single risk or protective factor has been identified that fully explains the observed trends, but major societal changes and improvements in living conditions, education and healthcare might have favourably influenced physical, mental and cognitive health throughout an individual’s
life course, and could be responsible for a reduced risk of dementia in later life. Analytical epidemiological approaches combined with translational neuroscientific research could provide a unique opportunity to explore the neuropathology that underlies changing occurrence of dementia in the general population.
||Hiroyuki Honda, Kosuke Matsuzono, Soichiro Fushimi, Kota Sato, Satoshi O Suzuki, Koji Abe, Toru Iwaki, C-Terminal-Deleted Prion Protein Fragment Is a Major Accumulated Component of Systemic PrP Deposits in Hereditary Prion Disease With a 2-bp (CT) Deletion in PRNP Codon 178, Journal of Neuropathology & Experimental Neurology, 2016.08.
||Masahiro Shijo, Hiroyuki Honda, Toru Iwaki, Dura mater graft-associated Creutzfeldt-Jakob disease with 30-year incubation period., Neuropathology, 10.1111/neup.12359., 37, 3, 275-281, 2016.11, Over 60% of all patients with dura mater graft-associated Creutzfeldt-Jakob disease (dCJD) have been diagnosed in Japan. The incubation period has ranged from 1 to 30 years and the age at onset from 15 to 80 years. Here, we report a 77-year-old male Japanese autopsied dCJD case with the longest incubation period so far in Japan. He received a cadaveric dural graft at the right cranial convexity following a craniotomy for meningioma at the age of 46. At 30 years post-dural graft placement, disorientation was observed as an initial symptom of dCJD. He rapidly began to present with inconsistent speech, cognitive impairment and tremor of the left upper extremity. Occasional myoclonic jerks were predominantly observed on the left side. Brain MRI presented hyperintense signals on diffusion-weighted and T2-weighted images, at the right cerebral cortex. The most hyperintense lesion was located at the right parietal lobe, where the dura mater graft had been transplanted. Single-photon emission CT scan showed markedly decreased cerebral blood flow at the right parietal lobe. EEG revealed diffuse and slow activities with periodic sharp-wave complex discharges seen in the right parietal, temporal and occipital lobes. He died of pneumonia 9 months after onset. Brain pathology revealed non-plaque-type dCJD. Laterality of neuropathological changes, including spongiform change, neuronal loss, gliosis or PrP deposits, was not evident. Western blot analysis showed type 1 PrPCJD . Alzheimer-type pathology and PSP-like pathology were also observed..
||Masahiro Shijo, Hiroyuki Honda, Satoshi O Suzuki, Toru Iwaki, Association of adipocyte enhancer-binding protein 1 with Alzheimer’s disease pathology in human hippocampi, Brain Pathology, 10.1111/bpa.12475., Epub ahead of print, 2016.12, Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF-jB pathway in macrophages and regulates adipogenesis in preadipocytes. Up-regulation of AEBP1 in the hippocampi of patients with Alzheimer’s disease (AD) has been revealed by microarray analyses of autopsied brains from the Japanese general population (the Hisayama study). In this study, we compared the expression patterns of AEBP1 in normal and AD brains, including in the hippocampus, using immunohistochemistry. The subjects were 24 AD cases and 52 non-AD cases. Brain specimens were immunostained with antibodies against AEBP1, tau protein, amyloid b protein, NF-jB, GFAP and Iba-1. In normal brains, AEBP1 immunoreactivity mainly localized to the perikarya of hippocampal pyramidal neurons, and its expression was elevated in the pyramidal neurons and some astrocytes in AD hippocampi. Although AEBP1 immunoreactivity was almost absent in neurons containing neurofibrillary tangles, AEBP1 was highly expressed in neurons with pretangles and in the tau-immunopositive, dystrophic neurites of senile plaques. .
||Hideomi Hamasaki, Hiroyuki Honda, Satoshi O Suzuki, Tomoyuki Ohara, Toshiharu Ninomiya, Toru Iwaki, Yutaka Kiyohara, Recent increases in hippocampal tau pathology in the aging Japanese population: the Hisayama study, Journal of Alzheimer's Disease, 2016.08.
||Hiroyuki Honda, Kensuke Sasaki, Hideomi Hamasaki, Masahiro Shijo, Tomoyuki Ohara, Toshiharu Ninomiya, Yutaka Kiyohara, Satoshi O Suzuki, Toru Iwaki, Trends in autopsy-verified dementia prevalence over 29 years of the Hisayama study., Neuropathology, 36, 4, 383-387, 2016.08.
||Kosuke Matsuzono, Hiroyuki Honda, Kota Sato, Ryuta Morihara, Toru Yamashita, Yasuyuki Ota, Koji Abe, Toru Iwaki, “PrP Systemic Deposition Disease”: Clinical and Pathological Characteristics of Novel Familial Prion Disease with 2-bp Deletion in Codon 178., European Journal of Neurology, in press, 2016.01.
||Hiroyuki Honda, Hideomi Hamasaki, Tomihiro Wakamiya, Satoshi O Suzuki, Naoki Fujii, Toru Iwaki, Loss of hnRNPA1 in ALS spinal cord motor neurons with TDP-43-positive inclusions, Neuropathology, 10.1111/neup.12153, 35, 1, 37-43, 2015.01.
||Hideomi Hamasaki, Hiroyuki Honda, Satoshi O Suzuki, Yutaka Kiyohara, Yusaku Nakabeppu, Toru Iwaki, Down-regulation of MET in hippocampal neurons of Alzheimer's disease brains, Neuropathology, 2014.08., Neuropathology, 2014.08.
||Hiroyuki Honda, Ryotaro Ishii, Ai Hamano, Kyoko Itoh, Satoshi O Suzuki, Shinji Fushiki, Masanori Nakagawa, Toru Iwaki, Microsphere formation in a subtype of Creutzfeldt-Jakob disease with a V180I mutation and codon 129 MM polymorphism., Neuropathology and Applied neurobiology, 2013.03.
||Honda H, Sasaki K, Minaki H, Masui K, Suzuki SO, Doh-Ura K, Iwaki T., Protease-resistant PrP and PrP oligomers in the brain in human prion diseases after intraventricular pentosan polysulfate infusion., Neuropathology, 2012.04.
||Haruhiko Minaki, Kensuke Sasaki, Hiroyuki Honda, Toru Iwaki, Prion protein oligomers in Creutzfeldt-Jakob disease detected by gel-filtration centrifuge columns., Neuropathology, 2009.10.