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  1. AU="Minatani, Shinobu"
  2. AU=Wang Yueying
  3. AU="Wagner, Holger"
  4. AU="Blinkey, Neil"
  5. AU=Jiang Yi

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  1. Artikel ; Online: Diffusion Mediates Molecular Transport through the Perivascular Space in the Brain.

    Tanaka, Marie / Hirayoshi, Yoko / Minatani, Shinobu / Hasegawa, Itsuki / Itoh, Yoshiaki

    International journal of molecular sciences

    2024  Band 25, Heft 5

    Abstract: The perivascular space has been proposed as a clearance pathway for degradation products in the brain, including amyloid β, the accumulation of which may induce Alzheimer's disease. Live images were acquired using a two-photon microscope through a closed ...

    Abstract The perivascular space has been proposed as a clearance pathway for degradation products in the brain, including amyloid β, the accumulation of which may induce Alzheimer's disease. Live images were acquired using a two-photon microscope through a closed cranial window in mice. In topical application experiments, the dynamics of FITC-dextran were evaluated from 30 to 150 min after the application and closure of the window. In continuous injection experiments, image acquisition began before the continuous injection of FITC-dextran. The transport of dextran molecules of different sizes was evaluated. In topical application experiments, circumferential accumulation around the penetrating arteries, veins, and capillaries was observed, even at the beginning of the observation period. No further increases were detected. In continuous injection experiments, a time-dependent increase in the fluorescence intensity was observed around the penetrating arteries and veins. Lower-molecular-weight dextran was transported more rapidly than higher-molecular-weight dextran, especially around the arteries. The largest dextran molecules were not transported significantly during the observation period. The size-dependent transport of dextran observed in the present study strongly suggests that diffusion is the main mechanism mediating substance transport in the perivascular space.
    Mesh-Begriff(e) Animals ; Mice ; Dextrans ; Amyloid beta-Peptides ; Brain ; Diffusion ; Fluorescein-5-isothiocyanate/analogs & derivatives
    Chemische Substanzen fluorescein isothiocyanate dextran ; Dextrans ; Amyloid beta-Peptides ; Fluorescein-5-isothiocyanate (I223NX31W9)
    Sprache Englisch
    Erscheinungsdatum 2024-02-20
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25052480
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: In Vivo Dynamic Movement of Polymerized Amyloid β in the Perivascular Space of the Cerebral Cortex in Mice.

    Hasegawa, Itsuki / Hirayoshi, Yoko / Minatani, Shinobu / Mino, Toshikazu / Takeda, Akitoshi / Itoh, Yoshiaki

    International journal of molecular sciences

    2022  Band 23, Heft 12

    Abstract: Disposition of amyloid β (Aβ) into the perivascular space of the cerebral cortex has been recently suggested as a major source of its clearance, and its disturbance may be involved in the pathogenesis of cerebral amyloid angiopathy and Alzheimer's ... ...

    Abstract Disposition of amyloid β (Aβ) into the perivascular space of the cerebral cortex has been recently suggested as a major source of its clearance, and its disturbance may be involved in the pathogenesis of cerebral amyloid angiopathy and Alzheimer's disease. Here, we explored the in vivo dynamics of Aβ in the perivascular space of anesthetized mice. Live images were obtained with two-photon microscopy through a closed cranial window. Either fluorescent-dye-labeled Aβ oligomers prepared freshly or Aβ fibrils after 6 days of incubation at 37 °C were placed over the cerebral cortex. Accumulation of Aβ was observed in the localized perivascular space of the penetrating arteries and veins. Transportation of the accumulated Aβ along the vessels was slow and associated with changes in shape. Aβ oligomers were transported smoothly and separately, whereas Aβ fibrils formed a mass and moved slowly. Parenchymal accumulation of Aβ oligomers, as well as Aβ fibrils along capillaries, increased gradually. In conclusion, we confirmed Aβ transportation between the cortical surface and the deeper parenchyma through the perivascular space that may be affected by the peptide polymerization. Facilitation of Aβ excretion through the system can be a key target in treating Alzheimer's disease.
    Mesh-Begriff(e) Alzheimer Disease/pathology ; Amyloid ; Amyloid beta-Peptides/metabolism ; Animals ; Brain/metabolism ; Cerebral Amyloid Angiopathy/pathology ; Cerebral Cortex/metabolism ; Mice ; Polymerization
    Chemische Substanzen Amyloid ; Amyloid beta-Peptides
    Sprache Englisch
    Erscheinungsdatum 2022-06-08
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23126422
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: An autopsy case of type A FTLD-TDP with a GRN mutation presenting with the logopenic variant of primary progressive aphasia at onset and with corticobasal syndrome subsequently.

    Tomenaga, Takafumi / Minatani, Shinobu / Namba, Hiroto / Takeda, Akitoshi / Yoshizaki, Takahito / Kawabe, Joji / Keyoumu, Nazere / Morino, Hiroyuki / Higuchi, Makoto / Matsubara, Tomoyasu / Hatsuta, Hiroyuki / Hasegawa, Masato / Murayama, Shigeo / Itoh, Yoshiaki

    Neuropathology : official journal of the Japanese Society of Neuropathology

    2024  

    Abstract: A 68-year-old woman presented with difficulty finding words and writing characters. Neurological examination led to clinical diagnosis at onset of the logopenic variant of primary progressive aphasia accompanied with ideomotor apraxia, visuospatial ... ...

    Abstract A 68-year-old woman presented with difficulty finding words and writing characters. Neurological examination led to clinical diagnosis at onset of the logopenic variant of primary progressive aphasia accompanied with ideomotor apraxia, visuospatial agnosia on the right, and Gerstmann syndrome. Bradykinesia and rigidity on the right with shuffling gait developed after one year. Treatment with L-dopa had no effect. The patient was diagnosed with corticobasal syndrome (CBS). Brain magnetic resonance imaging revealed diffuse cortical atrophy dominantly on the left, especially in the temporal, parietal, and occipital lobes. Positron emission tomography did not reveal any significant accumulation of amyloid β or tau protein. She died five years later. Neuropathological examination revealed diffuse cortical atrophy with severe neuronal loss and fibrous gliosis in the cortex. Neuronal cytoplasmic inclusions, short dystrophic neurites, and, most notably, neuronal intranuclear inclusions, all immunoreactive for phosphorylated TDP-43, were observed. Western blotting revealed a full length and fragments of phosphorylated TDP-43 at 45 and 23 kDa, respectively, confirming the pathological diagnosis of type A FTLD-TDP. Whole exome sequencing revealed a pathogenic mutation in GRN (c.87dupC). FTLD-TDP should be included in the differential diagnosis of CBS.
    Sprache Englisch
    Erscheinungsdatum 2024-05-07
    Erscheinungsland Australia
    Dokumenttyp Case Reports
    ZDB-ID 1483794-8
    ISSN 1440-1789 ; 0919-6544
    ISSN (online) 1440-1789
    ISSN 0919-6544
    DOI 10.1111/neup.12980
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Heavy Tau Burden with Subtle Amyloid β Accumulation in the Cerebral Cortex and Cerebellum in a Case of Familial Alzheimer's Disease with APP Osaka Mutation.

    Shimada, Hiroyuki / Minatani, Shinobu / Takeuchi, Jun / Takeda, Akitoshi / Kawabe, Joji / Wada, Yasuhiro / Mawatari, Aya / Watanabe, Yasuyoshi / Shimada, Hitoshi / Higuchi, Makoto / Suhara, Tetsuya / Tomiyama, Takami / Itoh, Yoshiaki

    International journal of molecular sciences

    2020  Band 21, Heft 12

    Abstract: We previously identified a novel mutation in amyloid precursor protein from a Japanese pedigree of familial Alzheimer's disease, FAD (Osaka). Our previous positron emission tomography (PET) study revealed that amyloid β (Aβ) accumulation was negligible ... ...

    Abstract We previously identified a novel mutation in amyloid precursor protein from a Japanese pedigree of familial Alzheimer's disease, FAD (Osaka). Our previous positron emission tomography (PET) study revealed that amyloid β (Aβ) accumulation was negligible in two sister cases of this pedigree, indicating a possibility that this mutation induces dementia without forming senile plaques. To further explore the relationship between Aβ, tau and neurodegeneration, we performed tau and Aβ PET imaging in the proband of FAD (Osaka) and in patients with sporadic Alzheimer's disease (SAD) and healthy controls (HCs). The FAD (Osaka) patient showed higher uptake of tau PET tracer in the frontal, lateral temporal, and parietal cortices, posterior cingulate gyrus and precuneus than the HCs (>2.5 SD) and in the lateral temporal and parietal cortices than the SAD patients (>2 SD). Most noticeably, heavy tau tracer accumulation in the cerebellum was found only in the FAD (Osaka) patient. Scatter plot analysis of the two tracers revealed that FAD (Osaka) exhibits a distinguishing pattern with a heavy tau burden and subtle Aβ accumulation in the cerebral cortex and cerebellum. These observations support our hypothesis that Aβ can induce tau accumulation and neuronal degeneration without forming senile plaques.
    Mesh-Begriff(e) Aged ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Cerebellum/metabolism ; Cerebellum/pathology ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Female ; Humans ; Male ; Middle Aged ; Mutation ; tau Proteins/metabolism
    Chemische Substanzen APP protein, human ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; MAPT protein, human ; tau Proteins
    Sprache Englisch
    Erscheinungsdatum 2020-06-22
    Erscheinungsland Switzerland
    Dokumenttyp Case Reports
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21124443
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Prevalence Estimates of Amyloid Abnormality Across the Alzheimer Disease Clinical Spectrum.

    Jansen, Willemijn J / Janssen, Olin / Tijms, Betty M / Vos, Stephanie J B / Ossenkoppele, Rik / Visser, Pieter Jelle / Aarsland, Dag / Alcolea, Daniel / Altomare, Daniele / von Arnim, Christine / Baiardi, Simone / Baldeiras, Ines / Barthel, Henryk / Bateman, Randall J / Van Berckel, Bart / Binette, Alexa Pichet / Blennow, Kaj / Boada, Merce / Boecker, Henning /
    Bottlaender, Michel / den Braber, Anouk / Brooks, David J / Van Buchem, Mark A / Camus, Vincent / Carill, Jose Manuel / Cerman, Jiri / Chen, Kewei / Chételat, Gaël / Chipi, Elena / Cohen, Ann D / Daniels, Alisha / Delarue, Marion / Didic, Mira / Drzezga, Alexander / Dubois, Bruno / Eckerström, Marie / Ekblad, Laura L / Engelborghs, Sebastiaan / Epelbaum, Stéphane / Fagan, Anne M / Fan, Yong / Fladby, Tormod / Fleisher, Adam S / Van der Flier, Wiesje M / Förster, Stefan / Fortea, Juan / Frederiksen, Kristian Steen / Freund-Levi, Yvonne / Frings, Lars / Frisoni, Giovanni B / Fröhlich, Lutz / Gabryelewicz, Tomasz / Gertz, Hermann-Josef / Gill, Kiran Dip / Gkatzima, Olymbia / Gómez-Tortosa, Estrella / Grimmer, Timo / Guedj, Eric / Habeck, Christian G / Hampel, Harald / Handels, Ron / Hansson, Oskar / Hausner, Lucrezia / Hellwig, Sabine / Heneka, Michael T / Herukka, Sanna-Kaisa / Hildebrandt, Helmut / Hodges, John / Hort, Jakub / Huang, Chin-Chang / Iriondo, Ane Juaristi / Itoh, Yoshiaki / Ivanoiu, Adrian / Jagust, William J / Jessen, Frank / Johannsen, Peter / Johnson, Keith A / Kandimalla, Ramesh / Kapaki, Elisabeth N / Kern, Silke / Kilander, Lena / Klimkowicz-Mrowiec, Aleksandra / Klunk, William E / Koglin, Norman / Kornhuber, Johannes / Kramberger, Milica G / Kuo, Hung-Chou / Van Laere, Koen / Landau, Susan M / Landeau, Brigitte / Lee, Dong Young / de Leon, Mony / Leyton, Cristian E / Lin, Kun-Ju / Lleó, Alberto / Löwenmark, Malin / Madsen, Karine / Maier, Wolfgang / Marcusson, Jan / Marquié, Marta / Martinez-Lage, Pablo / Maserejian, Nancy / Mattsson, Niklas / de Mendonça, Alexandre / Meyer, Philipp T / Miller, Bruce L / Minatani, Shinobu / Mintun, Mark A / Mok, Vincent C T / Molinuevo, Jose Luis / Morbelli, Silvia Daniela / Morris, John C / Mroczko, Barbara / Na, Duk L / Newberg, Andrew / Nobili, Flavio / Nordberg, Agneta / Olde Rikkert, Marcel G M / de Oliveira, Catarina Resende / Olivieri, Pauline / Orellana, Adela / Paraskevas, George / Parchi, Piero / Pardini, Matteo / Parnetti, Lucilla / Peters, Oliver / Poirier, Judes / Popp, Julius / Prabhakar, Sudesh / Rabinovici, Gil D / Ramakers, Inez H / Rami, Lorena / Reiman, Eric M / Rinne, Juha O / Rodrigue, Karen M / Rodríguez-Rodriguez, Eloy / Roe, Catherine M / Rosa-Neto, Pedro / Rosen, Howard J / Rot, Uros / Rowe, Christopher C / Rüther, Eckart / Ruiz, Agustín / Sabri, Osama / Sakhardande, Jayant / Sánchez-Juan, Pascual / Sando, Sigrid Botne / Santana, Isabel / Sarazin, Marie / Scheltens, Philip / Schröder, Johannes / Selnes, Per / Seo, Sang Won / Silva, Dina / Skoog, Ingmar / Snyder, Peter J / Soininen, Hilkka / Sollberger, Marc / Sperling, Reisa A / Spiru, Luisa / Stern, Yaakov / Stomrud, Erik / Takeda, Akitoshi / Teichmann, Marc / Teunissen, Charlotte E / Thompson, Louisa I / Tomassen, Jori / Tsolaki, Magda / Vandenberghe, Rik / Verbeek, Marcel M / Verhey, Frans R J / Villemagne, Victor / Villeneuve, Sylvia / Vogelgsang, Jonathan / Waldemar, Gunhild / Wallin, Anders / Wallin, Åsa K / Wiltfang, Jens / Wolk, David A / Yen, Tzu-Chen / Zboch, Marzena / Zetterberg, Henrik

    JAMA neurology

    2022  Band 79, Heft 3, Seite(n) 228–243

    Abstract: Importance: One characteristic histopathological event in Alzheimer disease (AD) is cerebral amyloid aggregation, which can be detected by biomarkers in cerebrospinal fluid (CSF) and on positron emission tomography (PET) scans. Prevalence estimates of ... ...

    Abstract Importance: One characteristic histopathological event in Alzheimer disease (AD) is cerebral amyloid aggregation, which can be detected by biomarkers in cerebrospinal fluid (CSF) and on positron emission tomography (PET) scans. Prevalence estimates of amyloid pathology are important for health care planning and clinical trial design.
    Objective: To estimate the prevalence of amyloid abnormality in persons with normal cognition, subjective cognitive decline, mild cognitive impairment, or clinical AD dementia and to examine the potential implications of cutoff methods, biomarker modality (CSF or PET), age, sex, APOE genotype, educational level, geographical region, and dementia severity for these estimates.
    Design, setting, and participants: This cross-sectional, individual-participant pooled study included participants from 85 Amyloid Biomarker Study cohorts. Data collection was performed from January 1, 2013, to December 31, 2020. Participants had normal cognition, subjective cognitive decline, mild cognitive impairment, or clinical AD dementia. Normal cognition and subjective cognitive decline were defined by normal scores on cognitive tests, with the presence of cognitive complaints defining subjective cognitive decline. Mild cognitive impairment and clinical AD dementia were diagnosed according to published criteria.
    Exposures: Alzheimer disease biomarkers detected on PET or in CSF.
    Main outcomes and measures: Amyloid measurements were dichotomized as normal or abnormal using cohort-provided cutoffs for CSF or PET or by visual reading for PET. Adjusted data-driven cutoffs for abnormal amyloid were calculated using gaussian mixture modeling. Prevalence of amyloid abnormality was estimated according to age, sex, cognitive status, biomarker modality, APOE carrier status, educational level, geographical location, and dementia severity using generalized estimating equations.
    Results: Among the 19 097 participants (mean [SD] age, 69.1 [9.8] years; 10 148 women [53.1%]) included, 10 139 (53.1%) underwent an amyloid PET scan and 8958 (46.9%) had an amyloid CSF measurement. Using cohort-provided cutoffs, amyloid abnormality prevalences were similar to 2015 estimates for individuals without dementia and were similar across PET- and CSF-based estimates (24%; 95% CI, 21%-28%) in participants with normal cognition, 27% (95% CI, 21%-33%) in participants with subjective cognitive decline, and 51% (95% CI, 46%-56%) in participants with mild cognitive impairment, whereas for clinical AD dementia the estimates were higher for PET than CSF (87% vs 79%; mean difference, 8%; 95% CI, 0%-16%; P = .04). Gaussian mixture modeling-based cutoffs for amyloid measures on PET scans were similar to cohort-provided cutoffs and were not adjusted. Adjusted CSF cutoffs resulted in a 10% higher amyloid abnormality prevalence than PET-based estimates in persons with normal cognition (mean difference, 9%; 95% CI, 3%-15%; P = .004), subjective cognitive decline (9%; 95% CI, 3%-15%; P = .005), and mild cognitive impairment (10%; 95% CI, 3%-17%; P = .004), whereas the estimates were comparable in persons with clinical AD dementia (mean difference, 4%; 95% CI, -2% to 9%; P = .18).
    Conclusions and relevance: This study found that CSF-based estimates using adjusted data-driven cutoffs were up to 10% higher than PET-based estimates in people without dementia, whereas the results were similar among people with dementia. This finding suggests that preclinical and prodromal AD may be more prevalent than previously estimated, which has important implications for clinical trial recruitment strategies and health care planning policies.
    Mesh-Begriff(e) Aged ; Alzheimer Disease/cerebrospinal fluid ; Alzheimer Disease/diagnostic imaging ; Alzheimer Disease/epidemiology ; Amyloid beta-Peptides/cerebrospinal fluid ; Amyloidogenic Proteins ; Amyloidosis ; Apolipoproteins E/genetics ; Biomarkers/cerebrospinal fluid ; Cognitive Dysfunction/diagnostic imaging ; Cognitive Dysfunction/epidemiology ; Cross-Sectional Studies ; Female ; Humans ; Male ; Middle Aged ; Peptide Fragments/cerebrospinal fluid ; Positron-Emission Tomography ; Prevalence ; tau Proteins/cerebrospinal fluid
    Chemische Substanzen Amyloid beta-Peptides ; Amyloidogenic Proteins ; Apolipoproteins E ; Biomarkers ; Peptide Fragments ; tau Proteins
    Sprache Englisch
    Erscheinungsdatum 2022-01-26
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2702023-X
    ISSN 2168-6157 ; 2168-6149
    ISSN (online) 2168-6157
    ISSN 2168-6149
    DOI 10.1001/jamaneurol.2021.5216
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Ui II Zs.191: Hefte anzeigen Standort:
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