Cited by 383Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

Recent advances in molecular pathways and therapeutic implications targeting neuroinflammation for Alzheimer’s disease

Open access
Dhapola, Rishika, Hota, Subhendu Shekhar, Sarma, Phulen, Bhattacharyya, Anusuya, Medhi, Bikash, Reddy, Dibbanti HariKrishna·2021·Inflammopharmacology

Abstract

Alzheimer's disease (AD) is a major contributor of dementia leading to the degeneration of neurons in the brain with major symptoms like loss of memory and learning. Many evidences suggest the involvement of neuroinflammation in the pathology of AD. Cytokines including TNF-α and IL-6 are also found increasing the BACE1 activity and expression of NFκB resulting in generation of Aβ in AD brain. Following the interaction of Aβ with microglia and astrocytes, other inflammatory molecules also get translocated to the site of inflammation by chemotaxis and exaggerate neuroinflammation. Various pathways like NFκB, p38 MAPK, Akt/mTOR, caspase, nitric oxide and COX trigger microglia to release inflammatory cytokines. PPARγ agonists like pioglitazone increases the phagocytosis of Aβ and reduces inflammatory cytokine IL-1β. Celecoxib and roficoxib like selective COX-2 inhibitors also ameliorate neuroinflammation. Non-selective COX inhibitor indomethacin is also potent inhibitor of inflammatory mediators released from microglia. Mitophagy process is considered quite helpful in reducing inflammation due to microglia as it promotes the phagocytosis of over activated microglial cells and other inflammatory cells. Mitophagy induction is also beneficial in the removal of damaged mitochondria and reduction of infiltration of inflammatory molecules at the site of accumulation of the damaged mitochondria. Targeting these pathways and eventually ameliorating the activation of microglia can mitigate neuroinflammation and come out as a better therapeutic option for the treatment of Alzheimer's disease.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1007/s10787-021-00889-6

Cites

61 of 61 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Dhapola, R., Hota, S. S., Sarma, P., Bhattacharyya, A., Medhi, B., & Reddy, D. H.
Affiliations
  • Central University of Punjab (IN)
  • Post Graduate Institute of Medical Education and Research (IN)
  • Government Medical College and Hospital (IN)
Venue
Inflammopharmacology
Published
2021-11-23
Volume
29
Issue
6
Pages
1669-1681
ISSN
  • 0925-4692 (ISSN-L)
  • 1568-5608
OpenAlex
W3215739089
Cited by
383
References
61
Citations by year
2026: 72 · 2025: 116 · 2024: 111 · 2023: 55 · 2022: 27 · 2020: 1
FWCI
5.64
Type
journal article
Language
en
Open access
Locations
  • Inflammopharmacology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
Alzheimer's disease, neuroinflammation, microglia, amyloid-beta, NF-κB, TNF-α, interleukin-6, p38 MAPK, caspases, nitric oxide, COX-2 inhibitors, PPARγ agonists, pioglitazone, celecoxib, rofecoxib, indomethacin, mitophagy, astrocytes
MeSH terms
Neuroinflammatory Diseases, Alzheimer Disease, Animals, Humans, Inflammation, Mitochondria, Cytokines, Inflammation Mediators, Molecular Targeted Therapy, Mitophagy

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review