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  1. Article ; Online: Connections between ApoE, sleep, and Aβ and tau pathologies in Alzheimer's disease.

    Sadleir, Katherine R / Vassar, Robert

    The Journal of clinical investigation

    2023  Volume 133, Issue 14

    Abstract: In this issue of the JCI, Wang and colleagues investigate the relationship between sleep disturbances, an environmental risk factor for Alzheimer's disease (AD), and the apolipoprotein 4 (APOEε4) allele, a strong genetic risk factor for AD. The authors ... ...

    Abstract In this issue of the JCI, Wang and colleagues investigate the relationship between sleep disturbances, an environmental risk factor for Alzheimer's disease (AD), and the apolipoprotein 4 (APOEε4) allele, a strong genetic risk factor for AD. The authors subjected an amyloid mouse model expressing human APOE3 or APOE4, with and without human AD-tau injection, to sleep deprivation and observed that amyloid and tau pathologies were worsened in the presence of APOE4. Moreover, decreased microglial clustering and increased dystrophic neurites around plaques were observed in sleep-deprived APOE4 mice. In addition, aquaporin 4, important for clearing amyloid-β through the glymphatic system, was reduced and less polarized to astrocytic endfeet. These APOE4-induced changes caused alterations in sleep behavior during recovery from sleep deprivation, suggesting a feed-forward cycle of sleep disturbance and increased AD pathology that can further disrupt sleep in the presence of APOE4.
    MeSH term(s) Animals ; Humans ; Mice ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/genetics ; Apolipoprotein E4/genetics ; Apolipoproteins E ; Mice, Transgenic ; Sleep Deprivation/genetics ; Sleep Deprivation/complications
    Chemical Substances Amyloid beta-Peptides ; Apolipoprotein E4 ; Apolipoproteins E ; Apoe protein, mouse
    Language English
    Publishing date 2023-07-17
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI171838
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  2. Article ; Online: Connections between ApoE, sleep, and Aβ and tau pathologies in Alzheimer’s disease

    Katherine R. Sadleir / Robert Vassar

    The Journal of Clinical Investigation, Vol 133, Iss

    2023  Volume 14

    Abstract: In this issue of the JCI, Wang and colleagues investigate the relationship between sleep disturbances, an environmental risk factor for Alzheimer’s disease (AD), and the apolipoprotein 4 (APOEε4) allele, a strong genetic risk factor for AD. The authors ... ...

    Abstract In this issue of the JCI, Wang and colleagues investigate the relationship between sleep disturbances, an environmental risk factor for Alzheimer’s disease (AD), and the apolipoprotein 4 (APOEε4) allele, a strong genetic risk factor for AD. The authors subjected an amyloid mouse model expressing human APOE3 or APOE4, with and without human AD-tau injection, to sleep deprivation and observed that amyloid and tau pathologies were worsened in the presence of APOE4. Moreover, decreased microglial clustering and increased dystrophic neurites around plaques were observed in sleep-deprived APOE4 mice. In addition, aquaporin 4, important for clearing amyloid-β through the glymphatic system, was reduced and less polarized to astrocytic endfeet. These APOE4-induced changes caused alterations in sleep behavior during recovery from sleep deprivation, suggesting a feed-forward cycle of sleep disturbance and increased AD pathology that can further disrupt sleep in the presence of APOE4.
    Keywords Medicine ; R
    Language English
    Publishing date 2023-07-01T00:00:00Z
    Publisher American Society for Clinical Investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Lower Cerebrospinal Fluid Amyloid-β

    Cahan, Joshua G / Vassar, Robert / Bonakdarpour, Borna

    Journal of Alzheimer's disease reports

    2023  Volume 7, Issue 1, Page(s) 641–647

    Abstract: Background: Cerebrospinal fluid (CSF) biomarkers of amyloid-β: Objective: Determine whether CSF biomarker levels aid prognostication of BPSD in AD.: Methods: This retrospective cohort study included patients over 65 with a diagnosis of AD based on ...

    Abstract Background: Cerebrospinal fluid (CSF) biomarkers of amyloid-β
    Objective: Determine whether CSF biomarker levels aid prognostication of BPSD in AD.
    Methods: This retrospective cohort study included patients over 65 with a diagnosis of AD based on CSF biomarkers. We measured time from CSF testing to the first antipsychotic use in the following months. We then analyzed time to antipsychotic (AP) use with respect to Aβ
    Results: Of 86 AD patients (average 72±5 years, 46.5% male), 11 patients (12.7%) received APs following CSF testing. Patients with Aβ
    Conclusion: These results suggest a relationship between lower CSF Aβ
    Language English
    Publishing date 2023-06-19
    Publishing country Netherlands
    Document type Journal Article
    ISSN 2542-4823
    ISSN (online) 2542-4823
    DOI 10.3233/ADR-220064
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  4. Article ; Online: The gut microbiome in Alzheimer's disease: what we know and what remains to be explored.

    Chandra, Sidhanth / Sisodia, Sangram S / Vassar, Robert J

    Molecular neurodegeneration

    2023  Volume 18, Issue 1, Page(s) 9

    Abstract: Alzheimer's disease (AD), the most common cause of dementia, results in a sustained decline in cognition. There are currently few effective disease modifying therapies for AD, but insights into the mechanisms that mediate the onset and progression of ... ...

    Abstract Alzheimer's disease (AD), the most common cause of dementia, results in a sustained decline in cognition. There are currently few effective disease modifying therapies for AD, but insights into the mechanisms that mediate the onset and progression of disease may lead to new, effective therapeutic strategies. Amyloid beta oligomers and plaques, tau aggregates, and neuroinflammation play a critical role in neurodegeneration and impact clinical AD progression. The upstream modulators of these pathological features have not been fully clarified, but recent evidence indicates that the gut microbiome (GMB) may have an influence on these features and therefore may influence AD progression in human patients. In this review, we summarize studies that have identified alterations in the GMB that correlate with pathophysiology in AD patients and AD mouse models. Additionally, we discuss findings with GMB manipulations in AD models and potential GMB-targeted therapeutics for AD. Lastly, we discuss diet, sleep, and exercise as potential modifiers of the relationship between the GMB and AD and conclude with future directions and recommendations for further studies of this topic.
    MeSH term(s) Animals ; Mice ; Humans ; Gastrointestinal Microbiome ; Alzheimer Disease ; Amyloid beta-Peptides ; Cognition ; Disease Models, Animal
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2023-02-01
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2244557-2
    ISSN 1750-1326 ; 1750-1326
    ISSN (online) 1750-1326
    ISSN 1750-1326
    DOI 10.1186/s13024-023-00595-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Seeds of Destruction: New Mechanistic Insights into the Role of Apolipoprotein E4 in Alzheimer's Disease.

    Vassar, Robert

    Neuron

    2017  Volume 96, Issue 5, Page(s) 953–955

    Abstract: Apolipoprotein E4 (apoE4) is the strongest genetic risk factor for Alzheimer's disease. Despite nearly 25 years of research, the mechanism by which apoE4 confers increased risk for Alzheimer's disease remains enigmatic. In this issue of Neuron, Liu et al. ...

    Abstract Apolipoprotein E4 (apoE4) is the strongest genetic risk factor for Alzheimer's disease. Despite nearly 25 years of research, the mechanism by which apoE4 confers increased risk for Alzheimer's disease remains enigmatic. In this issue of Neuron, Liu et al. (2017) and Huynh et al. (2017) shed new light on this important question.
    MeSH term(s) Alzheimer Disease ; Amyloidosis ; Apolipoprotein E4 ; Humans ; Neurons ; Problem Solving
    Chemical Substances Apolipoprotein E4
    Language English
    Publishing date 2017-12-07
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2017.11.022
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2496: Show issues Location:
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  6. Article ; Online: BACE1 inhibition as a therapeutic strategy for Alzheimer's disease.

    Vassar, Robert

    Journal of sport and health science

    2016  Volume 5, Issue 4, Page(s) 388–390

    Language English
    Publishing date 2016-10-21
    Publishing country China
    Document type Journal Article
    ZDB-ID 2673028-5
    ISSN 2213-2961 ; 2095-2546
    ISSN (online) 2213-2961
    ISSN 2095-2546
    DOI 10.1016/j.jshs.2016.10.004
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  7. Article ; Online: Biochemical Purification and Proteomic Characterization of Amyloid Fibril Cores from the Brain.

    Upadhyay, Arun / Vassar, Robert J / Savas, Jeffrey N

    Journal of visualized experiments : JoVE

    2022  , Issue 182

    Abstract: Proteinaceous fibrillar inclusions are key pathological hallmarks of multiple neurodegenerative diseases. In the early stages of Alzheimer's disease (AD), amyloid-beta peptides form protofibrils in the extracellular space, which act as seeds that ... ...

    Abstract Proteinaceous fibrillar inclusions are key pathological hallmarks of multiple neurodegenerative diseases. In the early stages of Alzheimer's disease (AD), amyloid-beta peptides form protofibrils in the extracellular space, which act as seeds that gradually grow and mature into large amyloid plaques. Despite this basic understanding, current knowledge of the amyloid fibril structure, composition, and deposition patterns in the brain is limited. One major barrier has been the inability to isolate highly purified amyloid fibrils from brain extracts. Affinity purification and laser capture microdissection-based approaches have been previously used to isolate amyloids but are limited by the small quantity of material that can be recovered. This novel, robust protocol describes the biochemical purification of amyloid plaque cores using sodium dodecyl sulfate (SDS) solubilization with sucrose density gradient ultracentrifugation and ultrasonication and yields highly pure fibrils from AD patients and AD model brain tissues. Mass spectrometry (MS)-based bottom-up proteomic analysis of the purified material represents a robust strategy to identify nearly all the primary protein components of amyloid fibrils. Previous proteomic studies of proteins in the amyloid coronae have revealed an unexpectedly large and functionally diverse collection of proteins. Notably, after refining the purification strategy, the number of co-purifying proteins was reduced by more than 10-fold, indicating the high purity of the isolated SDS insoluble material. Negative staining and immuno-gold electron microscopy allowed confirmation of the purity of these preparations. Further studies are required to understand the spatial and biological attributes that contribute to the deposition of these proteins into amyloid inclusions. Taken together, this analytical strategy is well-positioned to increase the understanding of amyloid biology.
    MeSH term(s) Alzheimer Disease/pathology ; Amyloid/chemistry ; Amyloid/metabolism ; Amyloid beta-Peptides/metabolism ; Brain/pathology ; Humans ; Plaque, Amyloid/pathology ; Proteomics/methods
    Chemical Substances Amyloid ; Amyloid beta-Peptides
    Language English
    Publishing date 2022-04-28
    Publishing country United States
    Document type Journal Article ; Video-Audio Media
    ZDB-ID 2259946-0
    ISSN 1940-087X ; 1940-087X
    ISSN (online) 1940-087X
    ISSN 1940-087X
    DOI 10.3791/63816
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  8. Article ; Online: Early detection and personalized medicine: Future strategies against Alzheimer's disease.

    Di Meco, Antonio / Vassar, Robert

    Progress in molecular biology and translational science

    2020  Volume 177, Page(s) 157–173

    Abstract: Alzheimer's disease (AD) is the leading cause of dementia and sixth cause of death in elderly adults. AD poses a huge economic burden on society and constitutes an unprecedented challenge for caregivers and families affected. Aging of the population is ... ...

    Abstract Alzheimer's disease (AD) is the leading cause of dementia and sixth cause of death in elderly adults. AD poses a huge economic burden on society and constitutes an unprecedented challenge for caregivers and families affected. Aging of the population is projected to drastically aggravate the situation in the near future. To date, no therapy is available to prevent or ameliorate the disease. Moreover, several clinical trials for promising therapeutic agents have failed. Lack of supporting biomarker data for pre-symptomatic enrollment and inaccurate stratification of patients based on genetic heterogeneity appear to be contributing factors to this lack of success. Recently, the treatment of cancer has seen enormous advances based on the personalized genetics and biomarkers of the individual patient, forming the foundation of precision medicine for cancer. Likewise, technological progress in AD biomarker research promises the availability of reliable assays for pathology staging on a routine basis relatively soon. Moreover, tremendous achievements in AD genetics and high-throughput genotyping technology allow identification of predisposing risk alleles accurately and on a large scale. Finally, availability of electronic health records (EHR) promises the opportunity to integrate biomarker, genomic and clinical data efficiently. Together, these advances will form the basis of precision medicine for AD.
    MeSH term(s) Aging ; Alzheimer Disease/diagnosis ; Alzheimer Disease/genetics ; Alzheimer Disease/therapy ; Biomarkers ; Humans ; Precision Medicine
    Chemical Substances Biomarkers
    Language English
    Publishing date 2020-12-03
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2471995-X
    ISSN 1878-0814 ; 0079-6603 ; 1877-1173
    ISSN (online) 1878-0814
    ISSN 0079-6603 ; 1877-1173
    DOI 10.1016/bs.pmbts.2020.10.002
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    Uc I Zs 357: Show issues Location:
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  9. Article ; Online: Modeling genetic diversity in Alzheimer's disease.

    Sadleir, Katherine R / Vassar, Robert

    Lab animal

    2019  Volume 48, Issue 3, Page(s) 87–88

    MeSH term(s) Alzheimer Disease/genetics ; Genetic Variation ; Humans
    Language English
    Publishing date 2019-02-02
    Publishing country United States
    Document type Journal Article ; Comment
    ISSN 1548-4475
    ISSN (online) 1548-4475
    DOI 10.1038/s41684-019-0248-3
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  10. Article: BACE1 inhibitor drugs in clinical trials for Alzheimer's disease.

    Vassar, Robert

    Alzheimer's research & therapy

    2014  Volume 6, Issue 9, Page(s) 89

    Abstract: β-site amyloid precursor protein cleaving enzyme 1 (BACE1) is the β-secretase enzyme required for the production of the neurotoxic β-amyloid (Aβ) peptide that is widely considered to have a crucial early role in the etiology of Alzheimer's disease (AD). ... ...

    Abstract β-site amyloid precursor protein cleaving enzyme 1 (BACE1) is the β-secretase enzyme required for the production of the neurotoxic β-amyloid (Aβ) peptide that is widely considered to have a crucial early role in the etiology of Alzheimer's disease (AD). As a result, BACE1 has emerged as a prime drug target for reducing the levels of Aβ in the AD brain, and the development of BACE1 inhibitors as therapeutic agents is being vigorously pursued. It has proven difficult for the pharmaceutical industry to design BACE1 inhibitor drugs that pass the blood-brain barrier, however this challenge has recently been met and BACE1 inhibitors are now in human clinical trials to test for safety and efficacy in AD patients and individuals with pre-symptomatic AD. Initial results suggest that some of these BACE1 inhibitor drugs are well tolerated, although others have dropped out because of toxicity and it is still too early to know whether any will be effective for the prevention or treatment of AD. Additionally, based on newly identified BACE1 substrates and phenotypes of mice that lack BACE1, concerns have emerged about potential mechanism-based side effects of BACE1 inhibitor drugs with chronic administration. It is hoped that a therapeutic window can be achieved that balances safety and efficacy. This review summarizes the current state of progress in the development of BACE1 inhibitor drugs and the evaluation of their therapeutic potential for AD.
    Language English
    Publishing date 2014-12-24
    Publishing country England
    Document type Journal Article
    ZDB-ID 2506521-X
    ISSN 1758-9193
    ISSN 1758-9193
    DOI 10.1186/s13195-014-0089-7
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