Evidence map›Paper›PMID 35149973›Full record

ReviewMolecular neurobiology2022

Microglia in Alzheimer's Disease: An Unprecedented Opportunity as Prospective Drug Target.

Bhargavi Kulkarni, Natália Cruz-Martins, Dileep Kumar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 33 citations in OpenAlex.

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  18. Physical Activity Rewires the Human Brain against Neurodegeneration.International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Bhargavi KulkarniPoona College of Pharmacy, Bharati Vidyapeeth (Deemed To Be University) Erandawane, Pune, 411038, Maharashtra, India.
Natália Cruz-MartinsInstitute of Research and Advanced, Training in Health Sciences and Technologies (CESPU), Rua Central de Gandra, 1317, 4585-116, Gandra, PRD, Portugal. ncmartins@med.up.pt.ORCID http://orcid.org/0000-0002-5934-5201
Dileep KumarPoona College of Pharmacy, Bharati Vidyapeeth (Deemed To Be University) Erandawane, Pune, 411038, Maharashtra, India. dileep.0@gmail.com.
Bharati Vidyapeeth Deemed University · INUniversidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is an ever more common neurodegenerative disease among the elderly, characterized by recurrent neuroinflammation and amyloid beta (Aβ) accumulation in the brain parenchyma. Recent genome-wide association studies (GWAS) have shown a distinct role for the innate immune system in AD, with microglia playing a key role. The function of microglial cells is stringently regulated by the neighboring microenvironment in the brain. Upon interruption in diseases, like AD, it demonstrates neurotoxic and neuroprotective action by M1 (neurotoxic) and M2 (neuroprotective) microglial phenotypes, respectively, in the brain. Microglial cells on activation by complement factors, toll-like receptors, and genetic variants result in Aβ' phagocytosis, synaptic pruning, and reactivation of complement pathway. Recent studies have demonstrated the presence of potential therapeutic targets in microglial cells. Immune receptors revealed on microglia as potential drug targets can be paired immunoglobulin-like type 2 receptor (PILR), CD3358, and triggering receptor expressed on myeloid cells 2 (TREM2), as they can have impact on late-onset AD occurrence and progression. Thus, targeting these receptors can accentuate the beneficial effects of microglial cells required to decelerate the progression of AD. This review emphasizes the microglial phenotypes, its function in AD brain, and potential immunological and therapeutic targets to fight this highly progressive neurodegenerative disorder.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAgedAmyloid beta-PeptidesBrainGenome-Wide Association StudyHumansMicrogliaAmyloid beta-PeptidesAmyloid beta depositionDrug targetsInnate immune systemMicrogliaTriggering receptor expressed on myeloid cells 2 (TREM2)

Identifiers

PMID35149973
OpenAlexW4211225114

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.