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  1. Article ; Online: ApoE4 makes microglia trem

    Heneka, Michael T

    Neuron

    2023  Volume 111, Issue 2, Page(s) 142–144

    Abstract: The ApoE-Trem2 pathway links two of the most important genetic risk variants for sporadic Alzheimer's disease. In this issue of Neuron, Gratuze and ... ...

    Abstract The ApoE-Trem2 pathway links two of the most important genetic risk variants for sporadic Alzheimer's disease. In this issue of Neuron, Gratuze and colleagues
    MeSH term(s) Animals ; Humans ; Mice ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Apolipoprotein E4/genetics ; Apolipoprotein E4/metabolism ; Apolipoproteins E/genetics ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Microglia/metabolism ; Phagocytosis ; Receptors, Immunologic/genetics ; Receptors, Immunologic/metabolism ; Mice, Transgenic
    Chemical Substances Apolipoprotein E4 ; Apolipoproteins E ; Membrane Glycoproteins ; Receptors, Immunologic ; Trem2 protein, mouse
    Language English
    Publishing date 2023-01-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2022.12.032
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2496: Show issues Location:
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  2. Article ; Online: The endotoxin hypothesis of Alzheimer's disease.

    Brown, Guy C / Heneka, Michael T

    Molecular neurodegeneration

    2024  Volume 19, Issue 1, Page(s) 30

    Abstract: Lipopolysaccharide (LPS) constitutes much of the surface of Gram-negative bacteria, and if LPS enters the human body or brain can induce inflammation and act as an endotoxin. We outline the hypothesis here that LPS may contribute to the pathophysiology ... ...

    Abstract Lipopolysaccharide (LPS) constitutes much of the surface of Gram-negative bacteria, and if LPS enters the human body or brain can induce inflammation and act as an endotoxin. We outline the hypothesis here that LPS may contribute to the pathophysiology of Alzheimer's disease (AD) via peripheral infections or gut dysfunction elevating LPS levels in blood and brain, which promotes: amyloid pathology, tau pathology and microglial activation, contributing to the neurodegeneration of AD. The evidence supporting this hypothesis includes: i) blood and brain levels of LPS are elevated in AD patients, ii) AD risk factors increase LPS levels or response, iii) LPS induces Aβ expression, aggregation, inflammation and neurotoxicity, iv) LPS induces TAU phosphorylation, aggregation and spreading, v) LPS induces microglial priming, activation and neurotoxicity, and vi) blood LPS induces loss of synapses, neurons and memory in AD mouse models, and cognitive dysfunction in humans. However, to test the hypothesis, it is necessary to test whether reducing blood LPS reduces AD risk or progression. If the LPS endotoxin hypothesis is correct, then treatments might include: reducing infections, changing gut microbiome, reducing leaky gut, decreasing blood LPS, or blocking LPS response.
    MeSH term(s) Mice ; Animals ; Humans ; Alzheimer Disease/metabolism ; Endotoxins/toxicity ; Endotoxins/metabolism ; Lipopolysaccharides ; Microglia/metabolism ; Inflammation/metabolism ; Amyloid beta-Peptides/metabolism
    Chemical Substances Endotoxins ; Lipopolysaccharides ; Amyloid beta-Peptides
    Language English
    Publishing date 2024-04-01
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2244557-2
    ISSN 1750-1326 ; 1750-1326
    ISSN (online) 1750-1326
    ISSN 1750-1326
    DOI 10.1186/s13024-024-00722-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Inflammasomes in neurological disorders - mechanisms and therapeutic potential.

    Ravichandran, Kishore Aravind / Heneka, Michael T

    Nature reviews. Neurology

    2024  Volume 20, Issue 2, Page(s) 67–83

    Abstract: Inflammasomes are molecular scaffolds that are activated by damage-associated and pathogen-associated molecular patterns and form a key element of innate immune responses. Consequently, the involvement of inflammasomes in several diseases that are ... ...

    Abstract Inflammasomes are molecular scaffolds that are activated by damage-associated and pathogen-associated molecular patterns and form a key element of innate immune responses. Consequently, the involvement of inflammasomes in several diseases that are characterized by inflammatory processes, such as multiple sclerosis, is widely appreciated. However, many other neurological conditions, including Alzheimer disease, Parkinson disease, amyotrophic lateral sclerosis, stroke, epilepsy, traumatic brain injury, sepsis-associated encephalopathy and neurological sequelae of COVID-19, all involve persistent inflammation in the brain, and increasing evidence suggests that inflammasome activation contributes to disease progression in these conditions. Understanding the biology and mechanisms of inflammasome activation is, therefore, crucial for the development of inflammasome-targeted therapies for neurological conditions. In this Review, we present the current evidence for and understanding of inflammasome activation in neurological diseases and discuss current and potential interventional strategies that target inflammasome activation to mitigate its pathological consequences.
    MeSH term(s) Humans ; Inflammasomes/metabolism ; Nervous System Diseases/drug therapy ; Stroke ; Multiple Sclerosis ; Brain/metabolism
    Chemical Substances Inflammasomes
    Language English
    Publishing date 2024-01-09
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2491514-2
    ISSN 1759-4766 ; 1759-4758
    ISSN (online) 1759-4766
    ISSN 1759-4758
    DOI 10.1038/s41582-023-00915-x
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  4. Article ; Online: Microglia heterogeneity in health and disease.

    Dadwal, Shilauni / Heneka, Michael T

    FEBS open bio

    2023  Volume 14, Issue 2, Page(s) 217–229

    Abstract: Microglia, the resident immune cells of the central nervous system (CNS), have received significant attention due to their critical roles in maintaining brain homeostasis and mediating cerebral immune responses. Understanding the origin of microglia has ... ...

    Abstract Microglia, the resident immune cells of the central nervous system (CNS), have received significant attention due to their critical roles in maintaining brain homeostasis and mediating cerebral immune responses. Understanding the origin of microglia has been a subject of great interest, and emerging evidence suggests that microglia consist of multiple subpopulations with unique molecular and functional characteristics. These subpopulations of microglia may exhibit specialized roles in response to different environmental cues as in disease conditions. The newfound understanding of microglial heterogeneity has significant implications for elucidating their roles in both physiological and pathological conditions. In the context of disease, microglia have been studied rigorously as they play a very important role in neuroinflammation. Dysregulated microglial activation and function contribute to chronic inflammation. Further exploration of microglial heterogeneity and their interactions with other cell types in the CNS will undoubtedly pave the way to novel therapeutic strategies targeting microglia-mediated pathologies. In this review, we discuss the latest advances in the field of microglia research, focusing specifically on the origin and subpopulations of microglia, the populations of microglia types in the brains of patients with neurodegenerative diseases, and how microglia are regulated in the healthy CNS.
    MeSH term(s) Humans ; Microglia ; Brain/pathology ; Inflammation ; Neurodegenerative Diseases ; Homeostasis
    Language English
    Publishing date 2023-11-16
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2651702-4
    ISSN 2211-5463 ; 2211-5463
    ISSN (online) 2211-5463
    ISSN 2211-5463
    DOI 10.1002/2211-5463.13735
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  5. Article ; Online: Chronic inflammation: a potential target in tauopathies.

    Ising, Christina / Heneka, Michael T

    The Lancet. Neurology

    2023  Volume 22, Issue 5, Page(s) 371–373

    MeSH term(s) Humans ; Tauopathies ; tau Proteins/metabolism ; Inflammation ; Brain/metabolism
    Chemical Substances tau Proteins
    Language English
    Publishing date 2023-04-13
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 2081241-3
    ISSN 1474-4465 ; 1474-4422
    ISSN (online) 1474-4465
    ISSN 1474-4422
    DOI 10.1016/S1474-4422(23)00116-3
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  6. Article ; Online: Immune Activation in Alzheimer Disease.

    Mary, Arnaud / Mancuso, Renzo / Heneka, Michael T

    Annual review of immunology

    2024  

    Abstract: Alzheimer disease (AD) is the most common neurodegenerative disease, and with no efficient curative treatment available, its medical, social, and economic burdens are expected to dramatically increase. AD is historically characterized by amyloid β (Aβ) ... ...

    Abstract Alzheimer disease (AD) is the most common neurodegenerative disease, and with no efficient curative treatment available, its medical, social, and economic burdens are expected to dramatically increase. AD is historically characterized by amyloid β (Aβ) plaques and tau neurofibrillary tangles, but over the last 25 years chronic immune activation has been identified as an important factor contributing to AD pathogenesis. In this article, we review recent and important advances in our understanding of the significance of immune activation in the development of AD. We describe how brain-resident macrophages, the microglia, are able to detect Aβ species and be activated, as well as the consequences of activated microglia in AD pathogenesis. We discuss transcriptional changes of microglia in AD, their unique heterogeneity in humans, and emerging strategies to study human microglia. Finally, we expose, beyond Aβ and microglia, the role of peripheral signals and different cell types in immune activation. Expected final online publication date for the
    Language English
    Publishing date 2024-02-29
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 604953-9
    ISSN 1545-3278 ; 0732-0582
    ISSN (online) 1545-3278
    ISSN 0732-0582
    DOI 10.1146/annurev-immunol-101921-035222
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  7. Article ; Online: Innate immune activation in neurodegenerative diseases.

    Castro-Gomez, Sergio / Heneka, Michael T

    Immunity

    2024  Volume 57, Issue 4, Page(s) 790–814

    Abstract: Activation of the innate immune system following pattern recognition receptor binding has emerged as one of the major pathogenic mechanisms in neurodegenerative disease. Experimental, epidemiological, pathological, and genetic evidence underscores the ... ...

    Abstract Activation of the innate immune system following pattern recognition receptor binding has emerged as one of the major pathogenic mechanisms in neurodegenerative disease. Experimental, epidemiological, pathological, and genetic evidence underscores the meaning of innate immune activation during the prodromal as well as clinical phases of several neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and frontotemporal dementia. Importantly, innate immune activation and the subsequent release of inflammatory mediators contribute mechanistically to other hallmarks of neurodegenerative diseases such as aberrant proteostatis, pathological protein aggregation, cytoskeleton abnormalities, altered energy homeostasis, RNA and DNA defects, and synaptic and network disbalance and ultimately to the induction of neuronal cell death. In this review, we discuss common mechanisms of innate immune activation in neurodegeneration, with particular emphasis on the pattern recognition receptors (PRRs) and other receptors involved in the detection of damage-associated molecular patterns (DAMPs).
    MeSH term(s) Humans ; Neurodegenerative Diseases ; Receptors, Pattern Recognition ; Immune System ; Inflammation Mediators ; Immunity, Innate
    Chemical Substances Receptors, Pattern Recognition ; Inflammation Mediators
    Language English
    Publishing date 2024-04-10
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2024.03.010
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  8. Article ; Online: An immune-cell signature marks the brain in Alzheimer's disease.

    Heneka, Michael T

    Nature

    2020  Volume 577, Issue 7790, Page(s) 322–323

    MeSH term(s) Alzheimer Disease ; Amyloid beta-Peptides ; Brain ; CD8-Positive T-Lymphocytes ; Humans
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2020-01-15
    Publishing country England
    Document type News ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-019-03892-8
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  9. Article ; Online: Microglia take centre stage in neurodegenerative disease.

    Heneka, Michael T

    Nature reviews. Immunology

    2019  Volume 19, Issue 2, Page(s) 79–80

    MeSH term(s) Animals ; Humans ; Microglia/pathology ; Neurodegenerative Diseases/pathology
    Language English
    Publishing date 2019-01-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-018-0112-5
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  10. Article ; Online: Inflammasome activation in neurodegenerative diseases.

    Ravichandran, Kishore Aravind / Heneka, Michael T

    Essays in biochemistry

    2021  Volume 65, Issue 7, Page(s) 885–904

    Abstract: Approximately ten million people are diagnosed with dementia annually since they experience difficulties with memory and thinking skills. Since neurodegenerative diseases are diagnosed late, most of them are difficult to treat. This is due to the ... ...

    Abstract Approximately ten million people are diagnosed with dementia annually since they experience difficulties with memory and thinking skills. Since neurodegenerative diseases are diagnosed late, most of them are difficult to treat. This is due to the increased severity of the disease during the progression when neuroinflammation plays a critical role. The activation of immune cells, especially microglia, plays a crucial role in the development of neurodegenerative diseases. Molecular sensors within these microglia, such as the NLRP3 inflammasome, are activated by signals that represent the hallmarks of neurodegenerative diseases. Here, we first summarize the two activation steps of NLRP3 inflammasome activation. Furthermore, we discuss the key factors that contribute to NLRP3 inflammasome activation in the different neuroinflammatory diseases, like Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). The prominent NLRP3 inflammasome triggers include amyloid β and tau oligomers in AD, α-synuclein in PD, and superoxide dismutase (SOD1) and TAR DNA-binding protein 43 (TDP43) in ALS. NLRP3 inhibitor treatment has shown promising results in several preclinical mouse models of AD, PD, and ALS. Finally, we postulate that current understandings underpin the potential for NLRP3 inhibitors as a therapeutic target in neurodegenerative diseases.
    MeSH term(s) Amyloid beta-Peptides/metabolism ; Animals ; Humans ; Inflammasomes/metabolism ; Mice ; Microglia/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Neurodegenerative Diseases/metabolism
    Chemical Substances Amyloid beta-Peptides ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein
    Language English
    Publishing date 2021-11-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1744-1358 ; 0071-1365
    ISSN (online) 1744-1358
    ISSN 0071-1365
    DOI 10.1042/EBC20210021
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