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Home › Research › Topic

Inflammation, microglia and astrocytes

730 studies in this group. A computer grouped them by what their titles and summaries are about, not by a hand-made list. The name describes most of the group, not every study in it.

Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.

Highest usefulness score first. Studies without a score come last.

  1. Identification and therapeutic modulation of a pro-inflammatory subset of disease-associated-microglia in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Molecular neurodegeneration 2018-05-21 Genetics

    Gene ontology analyses coupled with bioinformatics approaches revealed drug targets and transcriptional regulators of microglial modules predicted to favorably modulate neuroinflammation in AD.

  2. Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Frontiers in immunology 2018-04-09 Risk factors

    Cytokine dysregulation is believed to play a key role in the remodeling of the immune system at older age, with evidence pointing to an inability to fine-control systemic inflammation, which seems to be a marker of unsuccessful aging.

  3. White matter changes in Alzheimer's disease: a focus on myelin and oligodendrocytes

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Acta neuropathologica communications 2018-03-02 Disease mechanisms

    Alzheimer's disease (AD) is conceptualized as a progressive consequence of two hallmark pathological changes in grey matter: extracellular amyloid plaques and neurofibrillary tangles.

  4. Current Strategies for Brain Drug Delivery

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Theranostics 2018-02-05 Risk factors

    The blood-brain barrier (BBB) has been a great hurdle for brain drug delivery.

  5. Nuclear Factor-Kappa B and Alzheimer Disease, Unifying Genetic and Environmental Risk Factors from Cell to Humans

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Frontiers in immunology 2017-12-11 Treatments

    Alzheimer's disease (AD) is the most common form of dementia, an eversible, progressive disease that causes problems with memory, thinking, language, planning, and behavior.

  6. Temporal Tracking of Microglia Activation in Neurodegeneration at Single-Cell Resolution

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Cell reports 2017-10-01 Genetics

    Microglia, the tissue-resident macrophages in the brain, are damage sensors that react to nearly any perturbation, including neurodegenerative diseases such as Alzheimer's disease (AD).

  7. Antibiotic-induced perturbations in microbial diversity during post-natal development alters amyloid pathology in an aged APP SWE /PS1 ΔE9 murine model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Scientific reports 2017-09-05 Disease mechanisms

    Recent evidence suggests the commensal microbiome regulates host immunity and influences brain function; findings that have ramifications for neurodegenerative diseases.

  8. Microglia turnover with aging and in an Alzheimer's model via long-term in vivo single-cell imaging

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature neuroscience 2017-08-28 Genetics

    To clarify the role of microglia in brain homeostasis and disease, an understanding of their maintenance, proliferation and turnover is essential.

  9. Necroptosis activation in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature neuroscience 2017-07-24 Genetics

    Alzheimer's disease (AD) is characterized by severe neuronal loss; however, the mechanisms by which neurons die remain elusive.

  10. NRF2 deficiency replicates transcriptomic changes in Alzheimer's patients and worsens APP and TAU pathology

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Redox Biology 2017-07-04 Genetics

    Failure to translate successful neuroprotective preclinical data to a clinical setting in Alzheimer's disease (AD) indicates that amyloidopathy and tauopathy alone provide an incomplete view of disease.

  11. Human astrocytes in the diseased brain

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Brain research bulletin 2017-02-13 Down syndrome and Alzheimer's

    Astrocytes are key active elements of the brain that contribute to information processing.

  12. The role of peripheral immune cells in the CNS in steady state and disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature neuroscience 2017-01-16 Vascular contributions

    The CNS is protected by the immune system, including cells that reside directly within the CNS and help to ensure proper neural function, as well as cells that traffic into the CNS with disease.

  13. Gamma frequency entrainment attenuates amyloid load and modifies microglia

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2016-12-01 Inflammation and the immune system

    Changes in gamma oscillations (20-50 Hz) have been observed in several neurological disorders.

  14. The blood-brain barrier in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of disease 2016-07-15 Vascular contributions

    Alzheimer's disease (AD) is a chronic neurodegenerative disorder characterized by the pathological accumulation of amyloid beta (Aβ) peptides and neurofibrillary tangles containing hyperphosphorylated neuronal tau protein.

  15. Neutrophils promote Alzheimer's disease-like pathology and cognitive decline via LFA-1 integrin

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature medicine 2015-07-27 Brain tissue and pathology

    Inflammation is a pathological hallmark of Alzheimer's disease, and innate immune cells have been shown to contribute to disease pathogenesis.

  16. A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature medicine 2015-02-16 Risk factors

    The NOD-like receptor (NLR) family, pyrin domain-containing protein 3 (NLRP3) inflammasome is a component of the inflammatory process, and its aberrant activation is pathogenic in inherited disorders such as cryopyrin-associated periodic syndrome (CAPS) and complex diseases such as multiple sclerosis, type 2 diabetes, Alzheimer's disease and atherosclerosis.

  17. Prodromal Alzheimer's disease presenting as cerebral amyloid angiopathy-related inflammation with spontaneous amyloid-related imaging abnormalities and high cerebrospinal fluid anti-Aβ autoantibodies

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Alzheimer's disease : JAD 2015-01-01 Treatments

    Cerebral amyloid angiopathy-related inflammation (CAA-ri), a rare form of vasculitis associated with amyloid-β (Aβ) deposition in vessel walls, has been proposed as a spontaneous human model of the amyloid-related imaging abnormalities (ARIA) occurring after anti-Aβ immunotherapy for the treatment of Alzheimer's disease (AD).

  18. Anti-inflammatory therapy in chronic disease: challenges and opportunities

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 2013-01-01 Risk factors

    A number of widespread and devastating chronic diseases, including atherosclerosis, type 2 diabetes, and Alzheimer's disease, have a pathophysiologically important inflammatory component.

  19. ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 2012-02-09 Genetics

    Alzheimer's disease (AD) is associated with impaired clearance of β-amyloid (Aβ) from the brain, a process normally facilitated by apolipoprotein E (apoE).

  20. Dll4 signalling through Notch1 regulates formation of tip cells during angiogenesis

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2007-01-28 Brain scans and imaging

    In sprouting angiogenesis, specialized endothelial tip cells lead the outgrowth of blood-vessel sprouts towards gradients of vascular endothelial growth factor (VEGF)-A. VEGF-A is also essential for the induction of endothelial tip cells, but it is not known how single tip cells are selected to lead each vessel sprout, and how tip-cell numbers are determined.

  21. Differential modulation of endotoxin responsiveness by human caspase-12 polymorphisms

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2004-05-01 Disparities

    Caspases mediate essential key proteolytic events in inflammatory cascades and the apoptotic cell death pathway.

  22. Alzheimer's disease and angiogenesis

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Lancet (London, England) 2003-02-01 Drug development

    Despite enormous investigative efforts, the pathological basis for Alzheimer's disease remains unclear.

  23. Blockade of RAGE-amphoterin signalling suppresses tumour growth and metastases

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2000-05-01 Risk factors

    The receptor for advanced glycation end products (RAGE), a multi-ligand member of the immunoglobulin superfamily of cell surface molecules, interacts with distinct molecules implicated in homeostasis, development and inflammation, and certain diseases such as diabetes and Alzheimer's disease.

  24. Susac syndrome

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Medicine 1998-01-01 Risk factors

    Susac syndrome is an occlusive arteriolar disease that provokes infarcts in the cochlea, retina, and brain of young subjects, mostly women.

  25. Activation of microglial cells by beta-amyloid protein and interferon-gamma

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1995-04-01 Inflammation and the immune system

    Alzheimer's disease is the most common cause of progressive intellectual failure.

From across this topic

10 of the 730 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.

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