Nagoya University · Medicine
Professor Hiroshige Fujishiro's research lab specializes in the neuropathology and clinical progression of synucleinopathies, particularly dementia with Lewy bodies (DLB) and Parkinson's disease (PD). The lab focuses on understanding the histopathological correlates of early disease markers such as cardiac sympathetic denervation, REM sleep behavior disorder, and autonomic dysfunction, using immunohistochemical and imaging techniques. A central theme is the identification and validation of prodromal features that precede dementia, aiming to improve early diagnosis and pathophysiological understanding of Lewy body disease. The lab also investigates the neuropathological differences between familial and sporadic forms of Parkinson’s disease, especially in relation to α-synuclein and tau pathology.
Figures are computed from collected data and may differ slightly.
Attention has been drawn to cardiac sympathetic denervation in Parkinson's disease (PD) based on clinical studies using [123I] metaiodobenzylguanidine scintigraphy; however, the histologic correlates and time course of cardiac sympathetic denervation are poorly understood. To address these issues, we used tyrosine hydroxylase (TH) immunohistochemistry to detect cardiac sympathetic nerve fibers in the epicardium of 4 normal controls, 11 cases with incidental Lewy bodies (iLBs), and 14 cases of PD
There is limited information on the validity of the pathologic criteria of the Third Consortium on Dementia with Lewy bodies (CDLB), and none are based on prospectively diagnosed cases. In this study, the core clinical features of dementia with Lewy bodies (DLB) and the suggestive clinical feature of rapid eye movement sleep behavior disorder were assessed using a battery of standardized clinical instruments in 76 patients with the clinical diagnosis of either DLB or Alzheimer disease. At autops
Dementia with Lewy bodies (DLB) is defined pathologically as neurodegeneration associated with Lewy bodies (LB). LB-related symptoms, including olfactory dysfunction, dysautonomia, and mood and sleep disorders, are increasingly recognized as clinical signs that enable the early detection of DLB, because these symptoms often antedate dementia by years or even decades. It remains unknown if the clinical history of LB-related symptoms is sufficient for the prodromal state of DLB to be suspected in
Dementia with L ewy bodies ( DLB ) is the second most common neurodegenerative dementing disorder after A lzheimer's disease ( AD ), but there is limited information regarding the prodromal DLB state compared with that of AD . P arkinson's disease ( PD ) and DLB share common prodromal symptoms with L ewy body disease ( LBD ), allowing us to use a common strategy for identifying the individuals with an underlying pathophysiology of LBD . Dysautonomia, olfactory dysfunction, rapid eye movement sle
These variations in [(18) F]-FDG PET scans raise the possibility that the specific pattern of CMRglc reduction may predict developing DLB in patients with idiopathic RBD. Further follow-up studies are needed, particularly on patients with diffuse occipital hypometabolism.
The clinical features of the genetically determined forms of familial Parkinson's disease (PD) have been described in multiple reports, but there have been few comparative neuropathologic studies. Five familial PD cases, with mutations in SNCA, were matched for age, sex, and Alzheimer type pathology with sporadic PD cases. Immunohistochemistry for phospho-tau and α-synuclein was performed in 8 brain regions. The frequency of tau pathology and the morphologic features of α-synuclein pathology in
Glucose hypometabolism in the primary visual cortex is commonly associated with the clinical features of DLB regardless of cognitive conditions. Continued follow-up of these patients without dementia with the metabolic pattern is warranted to determine if they represent the prodromal state of DLB.
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