ReviewCurrent Alzheimer research2011
How to get from here to there: macrophage recruitment in Alzheimer's disease.
Review in Current Alzheimer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- Bridging the Gap: The Neuro-immune Axis as a Key Player in Neurodegenerative Disorders.Neuroscience bulletin · 2025Review
- Identification of immune-associated genes in vascular dementia by integrated bioinformatics and inflammatory infiltrates.Heliyon · 2024Article
- Article
- The effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of Alzheimer's disease.Neural regeneration research · 2023Review
- Hyperactivation of monocytes and macrophages in MCI patients contributes to the progression of Alzheimer's disease.Immunity & ageing : I & A · 2021Article
- Inflammasome NLRP3 Potentially Links Obesity-Associated Low-Grade Systemic Inflammation and Insulin Resistance with Alzheimer's Disease.International journal of molecular sciences · 2021Review
- The Role of the Inflammasome in Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2021Review
- The Role of Macrophage Migration Inhibitory Factor in Alzheimer's Disease: Conventionally Pathogenetic or Unconventionally Protective?Molecules (Basel, Switzerland) · 2020Review
- Longitudinal chemokine profile expression in a blood-brain barrier model from Alzheimer transgenic versus wild-type mice.Journal of neuroinflammation · 2018Article
- Immune and Imaging Correlates of Mild Cognitive Impairment Conversion to Alzheimer's Disease.Scientific reports · 2017Article
- Modulation of neuroinflammation and pathology in the 5XFAD mouse model of Alzheimer's disease using a biased and selective beta-1 adrenergic receptor partial agonist.Neuropharmacology · 2017Article
- Mathematical model on Alzheimer's disease.BMC systems biology · 2016Article
- The roles of inflammation and immune mechanisms in Alzheimer's disease.Alzheimer's & dementia (New York, N. Y.) · 2016Review
- Innate Immunity Fights Alzheimer's Disease.Trends in neurosciences · 2015Review
- Article
- Article
- Evaluation of inflammation-related genes polymorphisms in Mexican with Alzheimer's disease: a pilot study.Frontiers in cellular neuroscience · 2015Article
- Oxidized cholesterol as the driving force behind the development of Alzheimer's disease.Frontiers in aging neuroscience · 2015Review
- Interleukin-1β mediated amyloid plaque clearance is independent of CCR2 signaling in the APP/PS1 mouse model of Alzheimer's disease.Neurobiology of disease · 2014Article
- Multiple factors contribute to the peripheral induction of cerebral β-amyloidosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is pathologically defined by presence of intracellular neurofibrillary tangles and extracellular amyloid plaques comprised of amyoid-β (Aβ) peptides. Despite local recruitment of brain microglia to sites of amyloid deposition, these mononuclear phagocytes ultimately fail at restricting β-amyloid plaque formation. On the other hand, it is becoming increasingly clear that professional phagocytes from the periphery possess Aβ clearance aptitude. Yet, in order to harness this beneficial innate immune response, effective strategies must be developed to coax monocytes/macrophages from the periphery into the brain. It has previously been suggested that Aβ 'immunotherapy' clears cerebral Aβ deposits via mononuclear phagocytes, and recent evidence suggests that targeting transforming growth factor-β-Smad 2/3 signaling and chemokine pathways such as Ccr2 impacts blood-to-brain trafficking of these cells in transgenic mouse models of AD. It has also been shown that the fractalkine receptor (Cx3cr1) pathway plays a critical role in chemotaxis of mononuclear phagocytes toward neurons destined for death in AD model mice. In order to translate these basic science findings into AD treatments, a key challenge will be to develop a new generation of pharmacotherapeutics that safely and effectively promote recruitment of peripheral amyloid phagocytes into the AD brain.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.