Evidence map›Paper›PMID 34595669›Full record

ReviewMolecular neurobiology2021

Brain Exosomes: Friend or Foe in Alzheimer's Disease?

Sharanjot Kaur, Harkomal Verma, Monisha Dhiman, Gianluca Tell, Gian Luigi Gigli, Francesco Janes, Anil K Mantha

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Review
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  15. Specific Binding of Alzheimer's Aβ Peptides to Extracellular Vesicles.International journal of molecular sciences · 2024
    Article
  16. Review
  17. Article
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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

7 authors.

Sharanjot KaurDepartment of Microbiology, School of Biological Sciences , Central University of Punjab, Bathinda, Punjab, India.
Harkomal VermaDepartment of Zoology, School of Biological Sciences, Central University of Punjab, Village Ghudda151 401, Punjab, Bathinda, India.
Monisha DhimanDepartment of Microbiology, School of Biological Sciences , Central University of Punjab, Bathinda, Punjab, India.
Gianluca TellDepartment of Medicine, University of Udine, Udine, Italy.
Gian Luigi GigliDepartment of Medicine, University of Udine, Udine, Italy.
Francesco JanesClinical Neurology, Udine University Hospital, Udine, Italy.
Anil K ManthaDepartment of Zoology, School of Biological Sciences, Central University of Punjab, Village Ghudda151 401, Punjab, Bathinda, India. anil.mantha@cup.edu.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease. It is known to be a multifactorial disease and several causes are associated with its occurrence as well as progression. However, the accumulation of amyloid beta (Aβ) is widely considered its major pathogenic hallmark. Additionally, neurofibrillary tangles (NFT), mitochondrial dysfunction, oxidative stress, and aging (cellular senescence) are considered as additional hits affecting the disease pathology. Several studies are now suggesting important role of inflammation in AD, which shifts our thought towards the brain's resident immune cells, microglia, and astrocytes; how they interact with neurons; and how these interactions are affected by intra and extracellular stressful factors. These interactions can be modulated by different mechanisms and pathways, in which exosomes could play an important role. Exosomes are multivesicular bodies secreted by nearly all types of cells. The exosomes secreted by glial cells or neurons affect the interactions and thus the physiology of these cells by transmitting miRNAs, proteins, and lipids. Exosomes can serve as a friend or foe to the neuron function, depending upon the carried signals. Exosomes, from the healthy microenvironment, may assist neuron function and health, whereas, from the stressed microenvironment, they carry oxidative and inflammatory signals to the neurons and thus prove detrimental to the neuronal function. Furthermore, exosomes can cross the blood-brain barrier (BBB), and from the blood plasma they can enter the brain cells and activate microglia and astrocytes. Exosomes can transport Aβ or Tau, cytokines, miRNAs between the cells, and alter the physiology of recipient cells. They can also assist in Aβ clearance and regulation of synaptic activity. The exosomes derived from different cells play different roles, and this field is still in its infancy stage. This review advocates exosomes' role as a friend or foe in neurodegenerative diseases, especially in the case of Alzheimer's disease.

Indexed as

Alzheimer DiseaseAnimalsBrainExosomesHumansNeurofibrillary TanglesNeuronsPlaque, Amyloidtau Proteinstau ProteinsAlzheimer’s diseaseAβ plaqueExosomesNeurodegenerative diseaseNeurofibrillary tanglesTau

Identifiers

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.