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  1. Article ; Online: Correction to: The anti-cancer drug Sunitinib promotes autophagy and protects from neurotoxicity in an HIV-1 Tat model of neurodegeneration. Journal of NeuroVirology 2017.

    Masliah, Eliezer

    Journal of neurovirology

    2023  Volume 29, Issue 5, Page(s) 644

    Language English
    Publishing date 2023-10-09
    Publishing country United States
    Document type Letter
    ZDB-ID 1283265-0
    ISSN 1538-2443 ; 1355-0284
    ISSN (online) 1538-2443
    ISSN 1355-0284
    DOI 10.1007/s13365-023-01170-y
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  2. Book ; Online: Amyloid-beta clearance in Alzheimers disease

    Masliah, Eliezer / Marr, Robert

    2015  

    Abstract: Strong evidence continues to accumulate indicating that amyloid-beta (Aß) is a central part of Alzheimer's disease (AD) pathogenesis in spite of the negative evidence coming from failed clinical trials. Therefore, mechanisms of clearance of Aß are of ... ...

    Abstract Strong evidence continues to accumulate indicating that amyloid-beta (Aß) is a central part of Alzheimer's disease (AD) pathogenesis in spite of the negative evidence coming from failed clinical trials. Therefore, mechanisms of clearance of Aß are of great interest in understanding AD pathogenesis and the development of effective treatments. This topic focuses on the issues related to Aß clearance in AD. The topics covered include proteases that degrade Aß and their localization, regulation, and functions. This topic also covers issues related to clearance through uptake by glia and through low-density lipoprotein (LDL) receptor mediated mechanisms. Signal transduction related to AD pathology and clearance is also addressed. Finally, immunotherapy and other novel therapeutic approaches are discussed
    Keywords Neurosciences. Biological psychiatry. Neuropsychiatry ; Science (General)
    Size 1 electronic resource (111 p.)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT020090909
    ISBN 9782889194438 ; 2889194434
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  3. Article ; Online: Differential involvement of amyloidogenic evolvability in oligodendropathies; Multiple Sclerosis and Multiple System Atrophy.

    Wei, Jianshe / Ho, Gilbert / Masliah, Eliezer / Hashimoto, Makoto

    Prion

    2023  Volume 17, Issue 1, Page(s) 29–34

    Abstract: Although multiple sclerosis (MS) and multiple system atrophy (MSA) are both characterized by impaired oligodendrocytes (OLs), the aetiological relevance remains obscure. Given inherent stressors affecting OLs, the objective of the present study was to ... ...

    Abstract Although multiple sclerosis (MS) and multiple system atrophy (MSA) are both characterized by impaired oligodendrocytes (OLs), the aetiological relevance remains obscure. Given inherent stressors affecting OLs, the objective of the present study was to discuss the possible role of amyloidogenic evolvability (aEVO) in these conditions. Hypothetically, in aEVO, protofibrils of amyloidogenic proteins (APs), including β-synuclein and β-amyloid, might form in response to diverse stressors in parental brain. Subsequently, the AP protofibrils might be transmitted to offspring via germ cells in a prion-like fashion. By virtue of the stress information conferred by protofibrillar APs, the OLs in offspring's brain might be more resilient to forthcoming stressors, perhaps reducing MS risk. aEVO could be comparable to a gene for the inheritance of acquired characteristics. On the contrary, during ageing, MSA risk is increased through antagonistic pleiotropy. Consistently, the expression levels of APs are reduced in MS, but are increased in MSA compared to controls. Furthermore, β-synuclein, the non-amyloidogenic homologue of β-synuclein, might exert a buffering effect on aEVO, and abnormal β-synuclein could also increase MS and MSA disease activity. Collectively, a better understanding of the role of aEVO in the OL diseases might lead to novel interventions for such chronic degenerative conditions.
    MeSH term(s) Humans ; Multiple System Atrophy/genetics ; Multiple System Atrophy/metabolism ; alpha-Synuclein/genetics ; alpha-Synuclein/metabolism ; beta-Synuclein/metabolism ; Multiple Sclerosis/genetics ; Multiple Sclerosis/metabolism ; Brain/metabolism ; Amyloidogenic Proteins/genetics ; Amyloidogenic Proteins/metabolism
    Chemical Substances alpha-Synuclein ; beta-Synuclein ; Amyloidogenic Proteins
    Language English
    Publishing date 2023-02-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267671-5
    ISSN 1933-690X ; 1933-690X
    ISSN (online) 1933-690X
    ISSN 1933-690X
    DOI 10.1080/19336896.2023.2172912
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  4. Article ; Online: Cellular senescence and Alzheimer disease: the egg and the chicken scenario.

    Saez-Atienzar, Sara / Masliah, Eliezer

    Nature reviews. Neuroscience

    2020  Volume 21, Issue 8, Page(s) 433–444

    Abstract: Globally, 50 million people live with dementia, with Alzheimer disease (AD) being responsible for two-thirds of the total cases. As ageing is the main risk factor for dementia-related neurodegeneration, changes in the timing or nature of the cellular ... ...

    Abstract Globally, 50 million people live with dementia, with Alzheimer disease (AD) being responsible for two-thirds of the total cases. As ageing is the main risk factor for dementia-related neurodegeneration, changes in the timing or nature of the cellular hallmarks of normal ageing might be key to understanding the events that convert normal ageing into neurodegeneration. Cellular senescence is a candidate mechanism that might be important for this conversion. Under persistent stress, as occurs in ageing, both postmitotic cells - including neurons - and proliferative cells - such as astrocytes and microglia, among others - can engender a state of chronic cellular senescence that is characterized by the secretion of pro-inflammatory molecules that promote the functional decline of tissues and organs. Ablation of senescent cells has been postulated as a promising therapeutic venue to target the ageing phenotype and, thus, prevent or mitigate ageing-related diseases. However, owing to a lack of evidence, it is not possible to label cellular senescence as a cause or a consequence of neurodegeneration. This Review examines cellular senescence in the context of ageing and AD, and discusses which of the processes - cellular senescence or AD - might come first.
    MeSH term(s) Aging/pathology ; Aging/physiology ; Alzheimer Disease/pathology ; Alzheimer Disease/physiopathology ; Animals ; Cellular Senescence/physiology ; Humans
    Language English
    Publishing date 2020-06-29
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Review
    ZDB-ID 2034150-7
    ISSN 1471-0048 ; 1471-0048 ; 1471-003X
    ISSN (online) 1471-0048
    ISSN 1471-0048 ; 1471-003X
    DOI 10.1038/s41583-020-0325-z
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  5. Article ; Online: Author Correction: Cellular senescence and Alzheimer disease: the egg and the chicken scenario.

    Saez-Atienzar, Sara / Masliah, Eliezer

    Nature reviews. Neuroscience

    2020  Volume 21, Issue 10, Page(s) 587

    Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

    Abstract An amendment to this paper has been published and can be accessed via a link at the top of the paper.
    Language English
    Publishing date 2020-08-14
    Publishing country England
    Document type Journal Article ; Published Erratum
    ZDB-ID 2034150-7
    ISSN 1471-0048 ; 1471-0048 ; 1471-003X
    ISSN (online) 1471-0048
    ISSN 1471-0048 ; 1471-003X
    DOI 10.1038/s41583-020-0366-3
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  6. Article ; Online: Could changing the course of Alzheimer's disease pathology with immunotherapy prevent dementia?

    Overk, Cassia / Masliah, Eliezer

    Brain : a journal of neurology

    2019  Volume 142, Issue 7, Page(s) 1853–1855

    MeSH term(s) Alzheimer Disease ; Dementia ; Humans ; Immunization ; Immunotherapy ; Neuropathology
    Language English
    Publishing date 2019-09-12
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 80072-7
    ISSN 1460-2156 ; 0006-8950
    ISSN (online) 1460-2156
    ISSN 0006-8950
    DOI 10.1093/brain/awz165
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  7. Article ; Online: Specific Detection of Physiological S129 Phosphorylated α-Synuclein in Tissue Using Proximity Ligation Assay.

    Arlinghaus, Ryan / Iba, Michiyo / Masliah, Eliezer / Cookson, Mark R / Landeck, Natalie

    Journal of Parkinson's disease

    2023  Volume 13, Issue 2, Page(s) 255–270

    Abstract: Background: Synucleinopathies are a group of neurodegenerative disorders that are pathologically characterized by intracellular aggregates called Lewy bodies. Lewy bodies are primarily composed of α-synuclein (asyn) protein, which is mostly ... ...

    Abstract Background: Synucleinopathies are a group of neurodegenerative disorders that are pathologically characterized by intracellular aggregates called Lewy bodies. Lewy bodies are primarily composed of α-synuclein (asyn) protein, which is mostly phosphorylated at serine 129 (pS129) when aggregated and therefore used as a marker for pathology. Currently commercial antibodies against pS129 asyn stain aggregates well but in healthy brains cross react with other proteins, thus making it difficult to specifically detect physiological pS129 asyn.
    Objective: To develop a staining procedure that detects endogenous and physiological relevant pS129 asyn with high specificity and low background.
    Methods: We used the fluorescent and brightfield in situ proximity ligation assay (PLA) to specifically detect pS129 asyn in cell culture, mouse, and human brain sections.
    Results: The pS129 asyn PLA specifically stained physiological and soluble pS129 asyn in cell culture, mouse brain sections, and human brain tissue without significant cross-reactivity or background signal. However, this technique was not successful in detecting Lewy bodies in human brain tissue.
    Conclusion: We successfully developed a novel PLA method that can, in the future, be used on in vitro and in vivo samples as a tool to explore and better understand the cellular localization and function of pS129 asyn in health and disease.
    MeSH term(s) Animals ; Humans ; Mice ; alpha-Synuclein/metabolism ; Lewy Bodies/metabolism ; Parkinson Disease/diagnosis ; Phosphorylation ; Synucleinopathies/metabolism
    Chemical Substances alpha-Synuclein ; SNCA protein, human ; Snca protein, mouse
    Language English
    Publishing date 2023-02-27
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2620609-2
    ISSN 1877-718X ; 1877-7171
    ISSN (online) 1877-718X
    ISSN 1877-7171
    DOI 10.3233/JPD-213085
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    Zs.A 6964: Show issues Location:
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  8. Article ; Online: Novel systemic delivery of a peptide-conjugated antisense oligonucleotide to reduce α-synuclein in a mouse model of Alzheimer's disease.

    Leitão, André D G / Ahammad, Rijwan U / Spencer, Brian / Wu, Chengbiao / Masliah, Eliezer / Rissman, Robert A

    Neurobiology of disease

    2023  Volume 186, Page(s) 106285

    Abstract: Neurodegenerative disorders of aging are characterized by the progressive accumulation of proteins such as α-synuclein (α-syn) and amyloid beta (Aβ). Misfolded and aggregated α-syn has been implicated in neurological disorders such as Parkinson's disease, ...

    Abstract Neurodegenerative disorders of aging are characterized by the progressive accumulation of proteins such as α-synuclein (α-syn) and amyloid beta (Aβ). Misfolded and aggregated α-syn has been implicated in neurological disorders such as Parkinson's disease, and Dementia with Lewy Bodies, but less so in Alzheimer's Disease (AD), despite the fact that accumulation of α-syn has been confirmed in over 50% of postmortem brains neuropathologically diagnosed with AD. To date, no therapeutic strategy has effectively or consistently downregulated α-syn in AD. Here we tested the hypothesis that by using a systemically-delivered peptide (ApoB
    MeSH term(s) Animals ; Mice ; Oligonucleotides, Antisense/pharmacology ; alpha-Synuclein/genetics ; Alzheimer Disease/drug therapy ; Amyloid beta-Peptides ; Apolipoproteins B ; Disease Models, Animal
    Chemical Substances Oligonucleotides, Antisense ; alpha-Synuclein ; Amyloid beta-Peptides ; Apolipoproteins B
    Language English
    Publishing date 2023-09-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2023.106285
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  9. Article ; Online: Dale Schenk One Year Anniversary: Fighting to Preserve the Memories.

    Overk, Cassia / Masliah, Eliezer

    Journal of Alzheimer's disease : JAD

    2018  Volume 62, Issue 1, Page(s) 1–13

    Abstract: It has been a year since we lost Dale Schenk on September 30, 2016. Dale's visionary work resulted in the remarkable discovery in 1999 that an experimental amyloid-β (Aβ) vaccine reduced the neurodegeneration in a transgenic model of Alzheimer's disease ( ...

    Abstract It has been a year since we lost Dale Schenk on September 30, 2016. Dale's visionary work resulted in the remarkable discovery in 1999 that an experimental amyloid-β (Aβ) vaccine reduced the neurodegeneration in a transgenic model of Alzheimer's disease (AD). Following Dale's seminal work, several active and passive immunotherapies have since been developed and tested in the clinic for AD, Parkinson's disease (PD), and other neurodegenerative disorders. Here we provide a brief overview of the current state of development of immunotherapy for AD, PD, and other neurodegenerative disorders in the context of this anniversary. The next steps in the development of immunotherapies will require combinatorial approaches mixing antibodies against various targets (e.g., Aβ, α-syn, Tau, and TDP43) with small molecules that block toxicity, aggregation, inflammation, and promote cell survival.
    MeSH term(s) Anniversaries and Special Events ; History, 20th Century ; History, 21st Century ; Humans ; Immunotherapy ; Neurodegenerative Diseases/history ; Neurodegenerative Diseases/therapy ; United States
    Language English
    Publishing date 2018-02-10
    Publishing country Netherlands
    Document type Biography ; Historical Article ; Journal Article ; Portrait
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-171071
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  10. Article ; Online: NIA workshop on senescence in brain aging and Alzheimer's disease and its related dementias.

    DiBattista, Amanda M / Sierra, Felipe / Masliah, Eliezer

    GeroScience

    2020  Volume 42, Issue 2, Page(s) 389–396

    MeSH term(s) Aging ; Alzheimer Disease ; Brain ; Humans
    Language English
    Publishing date 2020-01-13
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2886586-8
    ISSN 2509-2723 ; 2509-2715
    ISSN (online) 2509-2723
    ISSN 2509-2715
    DOI 10.1007/s11357-020-00153-9
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