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  1. Article: Tau Propagation as a Diagnostic and Therapeutic Target for Dementia: Potentials and Unanswered Questions.

    Takeda, Shuko

    Frontiers in neuroscience

    2019  Volume 13, Page(s) 1274

    Abstract: A unique clinical course of Alzheimer's disease (AD), beginning with memory deficit as the earliest symptom, is well-correlated with a progressive pattern of intracellular aggregates of tau (neurofibrillary tangles), which spread from the medial temporal ...

    Abstract A unique clinical course of Alzheimer's disease (AD), beginning with memory deficit as the earliest symptom, is well-correlated with a progressive pattern of intracellular aggregates of tau (neurofibrillary tangles), which spread from the medial temporal lobe to other brain areas in a stereotypical manner. Recent findings from basic research using
    Language English
    Publishing date 2019-12-13
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2411902-7
    ISSN 1662-453X ; 1662-4548
    ISSN (online) 1662-453X
    ISSN 1662-4548
    DOI 10.3389/fnins.2019.01274
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  2. Article ; Online: Progression of Alzheimer's disease, tau propagation, and its modifiable risk factors.

    Takeda, Shuko

    Neuroscience research

    2018  Volume 141, Page(s) 36–42

    Abstract: The number of patients with Alzheimer's disease (AD) has been increasing exponentially side by side with aging societies worldwide. Symptoms of AD worsen over time due to progressive neurodegeneration, requiring institutional care at the later stage and ... ...

    Abstract The number of patients with Alzheimer's disease (AD) has been increasing exponentially side by side with aging societies worldwide. Symptoms of AD worsen over time due to progressive neurodegeneration, requiring institutional care at the later stage and resulting in a heavy burden on patients, caregivers, and the public-health system. AD neuropathology is characterized by cerebral accumulation and aggregation of amyloid-β (Aβ) and tau proteins. For decades, Aβ has been a leading target in the therapeutic development for AD, and many drug candidates have been tested in clinical trials; however, most medications have failed to slow the progression of the disease. Tau pathology currently is attracting more attention as an alternate target for developing disease-modifying therapy. Tau is known to spread in a hierarchical pattern in AD brain, likely by trans-synaptic tau transfer between neurons. Extracellular tau may mediate tau spreading and serve as biomarker for AD. AD pathogenesis is multifactorial, and many genetic- and non-genetic factors are known to contribute to Aβ- and tau-related pathology. Recent studies indicate an association between vascular risk factors and AD. Identifying modifiable risk factors for AD and understanding their contributory mechanisms could be key in tackling this devastating disease.
    MeSH term(s) Alzheimer Disease/cerebrospinal fluid ; Alzheimer Disease/complications ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Animals ; Biomarkers/cerebrospinal fluid ; Brain/metabolism ; Brain/pathology ; Disease Progression ; Humans ; Neurofibrillary Tangles/metabolism ; Neurofibrillary Tangles/pathology ; Risk Factors ; tau Proteins/metabolism
    Chemical Substances Amyloid beta-Peptides ; Biomarkers ; tau Proteins
    Language English
    Publishing date 2018-08-16
    Publishing country Ireland
    Document type Journal Article ; Review
    ZDB-ID 605842-5
    ISSN 1872-8111 ; 0168-0102 ; 0921-8696
    ISSN (online) 1872-8111
    ISSN 0168-0102 ; 0921-8696
    DOI 10.1016/j.neures.2018.08.005
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    Zs.A 1993: Show issues Location:
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  3. Article ; Online: Peripheral Aβ acts as a negative modulator of insulin secretion.

    Shigemori, Keiko / Nomura, Sachiko / Umeda, Tomohiro / Takeda, Shuko / Tomiyama, Takami

    Proceedings of the National Academy of Sciences of the United States of America

    2022  Volume 119, Issue 12, Page(s) e2117723119

    Abstract: Type 2 diabetes mellitus is known to be a risk factor for Alzheimer’s disease (AD), but the underlying mechanisms remain unclear. In AD, the cerebral accumulation of amyloid β (Aβ) triggers a pathological cascade leading to neurodegeneration. Plasma Aβ ... ...

    Abstract Type 2 diabetes mellitus is known to be a risk factor for Alzheimer’s disease (AD), but the underlying mechanisms remain unclear. In AD, the cerebral accumulation of amyloid β (Aβ) triggers a pathological cascade leading to neurodegeneration. Plasma Aβ levels are thought to reflect the brain amyloid pathology and currently used as a diagnostic biomarker of AD. However, amyloid precursor protein and Aβ-generating enzymes, β- and γ-secretases, are widely expressed in various peripheral tissues. Previous reports have shown that glucose and insulin loading cause a transient increase of plasma Aβ in mice and humans. These findings led us to speculate that plasma Aβ is produced from glucose- and insulin-susceptible peripheral tissues to play a role in glucose and insulin metabolism. To test this hypothesis, we investigated the effects of glucose and insulin on Aβ secretion and the effect of Aβ on insulin secretion in vivo, ex vivo, and in vitro. Aβ was found to be secreted from β-cells of the pancreas along with insulin upon glucose stimulation. Upon insulin stimulation, Aβ was secreted from cells of insulin-targeted organs, such as adipose tissues, skeletal muscles, and the liver, along with their organokines. Furthermore, Aβ inhibited the glucose-triggered insulin secretion from β-cells, slowing down glucose clearance from the blood. These results suggest that peripheral Aβ acts as a negative modulator of insulin secretion. Our findings provide a possible mechanism linking diabetes to AD and call attention to how plasma Aβ levels are used in AD diagnosis.
    MeSH term(s) Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Brain/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Glucose/metabolism ; Humans ; Insulin/metabolism ; Insulin Secretion
    Chemical Substances Amyloid beta-Peptides ; Insulin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2022-03-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2117723119
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  4. Article: [Pathological interaction between diabetes mellitus and Alzheimer's disease].

    Takeda, Shuko

    Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology

    2012  Volume 32, Issue 5-6, Page(s) 239–244

    Abstract: The incidence of dementia and diabetes mellitus is increasing at an alarming rate, and has become a major public health concern all over the world. Recent epidemiological studies suggest that the risk of Alzheimer's disease is increased in individuals ... ...

    Abstract The incidence of dementia and diabetes mellitus is increasing at an alarming rate, and has become a major public health concern all over the world. Recent epidemiological studies suggest that the risk of Alzheimer's disease is increased in individuals with diabetes mellitus, although the underlying mechanisms remain largely unknown. To analyze underlying mechanisms linking Alzheimer's disease and diabetes mellitus, we established unique animal models that show pathological manifestations of both diseases. Our findings suggest that impaired brain insulin signaling and cerebrovascular changes could be potential underlying mechanisms for this relationship. On the other hand, interestingly, Alzheimer's amyloid pathology aggravated diabetes mellitus in these mouse models, suggesting the presence of mutual interaction between these diseases. In addition, we also found that plasma Abeta levels rapidly and strikingly increased after glucose loading in Alzheimer's disease mouse models, which could be a novel diagnostic marker of Alzheimer's disease. The current review summarizes the results of our recent studies on the pathological relationship between these diseases, which could provide novel insights into this intensely debated association.
    MeSH term(s) Alzheimer Disease/etiology ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid/metabolism ; Animals ; Diabetes Complications/blood ; Diabetes Complications/pathology ; Disease Models, Animal ; Humans ; Insulin/blood
    Chemical Substances Amyloid ; Insulin
    Language Japanese
    Publishing date 2012-11
    Publishing country Japan
    Document type English Abstract ; Journal Article ; Review
    ZDB-ID 1285665-4
    ISSN 1340-2544
    ISSN 1340-2544
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  5. Article ; Online: Imaging Biomarker for Early-Stage Alzheimer Disease: Utility of Hippocampal Histogram Analysis of Diffusion Metrics.

    Takahashi, Hiroto / Takami, Yoichi / Takeda, Shuko / Hayakawa, Naoki / Nakajima, Tsuneo / Takeya, Yasushi / Matsuo-Hagiyama, Chisato / Arisawa, Atsuko / Rakugi, Hiromi / Tomiyama, Noriyuki

    AJNR. American journal of neuroradiology

    2024  Volume 45, Issue 3, Page(s) 320–327

    Abstract: Background and purpose: Biomarkers have been required for diagnosing early Alzheimer disease. We assessed the utility of hippocampal diffusion parameters for diagnosing Alzheimer disease pathology in mild cognitive impairment.: Materials and methods: ...

    Abstract Background and purpose: Biomarkers have been required for diagnosing early Alzheimer disease. We assessed the utility of hippocampal diffusion parameters for diagnosing Alzheimer disease pathology in mild cognitive impairment.
    Materials and methods: Sixty-nine patients with mild cognitive impairment underwent both CSF measurement and multi-shell diffusion imaging at 3T. Based on the CSF biomarker level, patients were classified according to the presence (Alzheimer disease group,
    Results: Most intraclass correlation coefficient values were between 0.59 and 0.91. In the regions of interest of both observers, there were statistically significant intergroup differences for the left-side neurite orientation dispersion and density imaging-derived intracellular volume fraction, right-side diffusion tensor imaging-derived mean diffusivity, left-side diffusion tensor imaging-derived mean diffusivity, axial diffusivity, and radial diffusivity (
    Conclusions: Hippocampal diffusion parameters might be useful for the early diagnosis of Alzheimer disease.
    MeSH term(s) Humans ; Alzheimer Disease/pathology ; Diffusion Tensor Imaging/methods ; Diffusion Magnetic Resonance Imaging/methods ; Hippocampus/diagnostic imaging ; Hippocampus/pathology ; Biomarkers
    Chemical Substances Biomarkers
    Language English
    Publishing date 2024-03-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 603808-6
    ISSN 1936-959X ; 0195-6108
    ISSN (online) 1936-959X
    ISSN 0195-6108
    DOI 10.3174/ajnr.A8106
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  6. Article ; Online: Roles of vascular risk factors in the pathogenesis of dementia.

    Takeda, Shuko / Rakugi, Hiromi / Morishita, Ryuichi

    Hypertension research : official journal of the Japanese Society of Hypertension

    2019  Volume 43, Issue 3, Page(s) 162–167

    Abstract: The number of people with dementia is rapidly growing along with the aging of society and is becoming a social issue worldwide. The results of recent clinical and basic studies have suggested that vascular risk factors, such as hypertension and diabetes ... ...

    Abstract The number of people with dementia is rapidly growing along with the aging of society and is becoming a social issue worldwide. The results of recent clinical and basic studies have suggested that vascular risk factors, such as hypertension and diabetes mellitus, affect the pathogenesis of dementia. Cerebrovascular damage due to vascular risk factors directly triggers vascular dementia, and it is becoming more apparent that vascular risk factors also increase the risk of neurodegenerative Alzheimer's disease, which is associated with the accumulation of neurotoxic proteins in the brain. Although disease-modifying therapy for dementia has not yet been established, several studies have shown that the management of vascular risk factors could possibly contribute to reducing the risk of developing dementia, thus making them important targets for dementia prevention. In this article, we review recent findings regarding the relationship between vascular risk factors and dementia, especially focusing on Alzheimer's disease, the underlying molecular mechanisms, and the potential strategies targeting these modifiable risk factors to prevent cognitive decline.
    MeSH term(s) Blood Pressure/physiology ; Cognitive Dysfunction/etiology ; Cognitive Dysfunction/physiopathology ; Dementia/etiology ; Dementia/physiopathology ; Humans ; Hypertension/complications ; Hypertension/physiopathology ; Risk Factors
    Language English
    Publishing date 2019-11-14
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1175297-x
    ISSN 1348-4214 ; 0916-9636
    ISSN (online) 1348-4214
    ISSN 0916-9636
    DOI 10.1038/s41440-019-0357-9
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  7. Article ; Online: Angiotensin Receptor Blocker Protects Alzheimer's Disease Brain From Ischemic Insult.

    Takeda, Shuko / Morishita, Ryuichi

    American journal of hypertension

    2016  Volume 30, Issue 2, Page(s) 110–111

    MeSH term(s) Alzheimer Disease ; Angiotensin Receptor Antagonists ; Animals ; Brain ; Cognitive Dysfunction ; Mice ; Receptor, Angiotensin, Type 1
    Chemical Substances Angiotensin Receptor Antagonists ; Receptor, Angiotensin, Type 1
    Language English
    Publishing date 2016-12-08
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 639383-4
    ISSN 1941-7225 ; 1879-1905 ; 0895-7061
    ISSN (online) 1941-7225 ; 1879-1905
    ISSN 0895-7061
    DOI 10.1093/ajh/hpw158
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    Zs.A 2329: Show issues Location:
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  8. Article: Ultrasound attacks Alzheimer's disease?

    Takeda, Shuko / Morishita, Ryuichi

    Annals of translational medicine

    2015  Volume 3, Issue 18, Page(s) 276

    Language English
    Publishing date 2015-10-30
    Publishing country China
    Document type Journal Article
    ZDB-ID 2893931-1
    ISSN 2305-5847 ; 2305-5839
    ISSN (online) 2305-5847
    ISSN 2305-5839
    DOI 10.3978/j.issn.2305-5839.2015.09.21
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  9. Article ; Online: Antiepileptic Drugs Modulate Alzheimer-Related Tau Aggregation in a Neuronal Activity-Independent Manner.

    Ito, Yuki / Takeda, Shuko / Moroi, Sayaka / Nakajima, Tsuneo / Oyama, Akane / Miki, Kunihiro / Sugihara, Nanami / Takami, Yoichi / Takeya, Yasushi / Shimamura, Munehisa / Rakugi, Hiromi / Morishita, Ryuichi

    Dementia and geriatric cognitive disorders

    2023  Volume 52, Issue 2, Page(s) 108–116

    Abstract: Introduction: A rapidly increasing number of patients with dementia present a serious social problem. Recently, the incidence of epilepsy in patients with Alzheimer's disease (AD) is increasing, drawing attention to the pathological relationship between ...

    Abstract Introduction: A rapidly increasing number of patients with dementia present a serious social problem. Recently, the incidence of epilepsy in patients with Alzheimer's disease (AD) is increasing, drawing attention to the pathological relationship between the two conditions. Clinical studies have suggested the protective action of antiepileptic agents on dementia; however, the underlying mechanism remains unknown. We evaluated the effects of multiple antiepileptic drugs using tau aggregation assay systems to determine the effects of antiepileptic agents on tau aggregation, a major neuropathological finding associated with AD.
    Methods: We evaluated the effects of seven antiepileptic agents on intracellular tau aggregation using a tau-biosensor cell-based high-throughput assay. Next, we tested these agents in a cell-free tau aggregation assay using thioflavin T (ThT).
    Results: The assay results revealed that phenobarbital inhibited tau aggregation, whereas sodium valproate, gabapentin, and piracetam promoted tau aggregation. In the cell-free tau aggregation assay using ThT, we confirmed that phenobarbital significantly inhibited tau aggregation.
    Conclusion: Antiepileptic drugs may modify the tau pathology in AD in a neural activity-independent manner. Our finding may provide an important insight into the optimization of antiepileptic drug therapy in older adults with dementia.
    MeSH term(s) Humans ; Aged ; Anticonvulsants/pharmacology ; Anticonvulsants/therapeutic use ; Alzheimer Disease/drug therapy ; Alzheimer Disease/pathology ; tau Proteins ; Valproic Acid/pharmacology ; Valproic Acid/therapeutic use ; Phenobarbital/therapeutic use
    Chemical Substances Anticonvulsants ; tau Proteins ; Valproic Acid (614OI1Z5WI) ; Phenobarbital (YQE403BP4D)
    Language English
    Publishing date 2023-03-06
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1026007-9
    ISSN 1421-9824 ; 1013-7424
    ISSN (online) 1421-9824
    ISSN 1013-7424
    DOI 10.1159/000529915
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    Zs.A 2866: Show issues Location:
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  10. Article ; Online: Effect of heat stress on blood-brain barrier integrity in iPS cell-derived microvascular endothelial cell models.

    Yamaguchi, Tomoko / Shimizu, Kentaro / Kokubu, Yasuhiro / Nishijima, Misae / Takeda, Shuko / Ogura, Hiroshi / Kawabata, Kenji

    PloS one

    2019  Volume 14, Issue 9, Page(s) e0222113

    Abstract: The incidence of heatstroke has been increasing. Heatstroke has been shown to affect physiological barrier functions. However, there are few studies of the effect of heat stress on the blood-brain barrier (BBB) function. In this study, we investigated ... ...

    Abstract The incidence of heatstroke has been increasing. Heatstroke has been shown to affect physiological barrier functions. However, there are few studies of the effect of heat stress on the blood-brain barrier (BBB) function. In this study, we investigated the influence of heat stress on brain microvascular endothelial cells in vivo and in vitro. Heatstroke model mice administered Texas Red-dextran showed leakage outside the brain vessel walls. In addition, trans-endothelial electrical resistance (TEER) value was significantly reduced in induced pluripotent stem (iPS) cell-derived brain microvascular endothelial cells under heat stress by reducing claudin-5 expression. In addition, our results showed that the expression level of P-glycoprotein (P-gp) was increased in iPS cell-derived brain microvascular endothelial cells under heat stress. Furthermore, serum from heatstroke model mice could impair the BBB integrity of iPS cell-derived brain microvascular endothelial cells. These results suggest that BBB integrity was affected by heat stress in vivo and in vitro and provide important insights into the development of new therapeutic strategies for heatstroke patients.
    MeSH term(s) Animals ; Blood-Brain Barrier/metabolism ; Cell Line ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Heat-Shock Response ; Induced Pluripotent Stem Cells/cytology ; Mice ; Mice, Inbred C57BL ; Microvessels/cytology ; Permeability
    Language English
    Publishing date 2019-09-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0222113
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