Evidence map›Paper›PMID 34699027›Full record

ReviewMolecular neurobiology2022

Implications of Phosphoinositide 3-Kinase-Akt (PI3K-Akt) Pathway in the Pathogenesis of Alzheimer's Disease.

Manish Kumar, Nitin Bansal

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 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
19.2field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 186 citations in OpenAlex.

  1. Review
  2. Article
  3. Abscisic Acid Enhances Hippocampal Neuroplasticity and Rescues Learning and Memory Deficits in a Valproate-Induced Rat Model of Autism.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2026
    Article
  4. Article
  5. CSF proteome-wide study of neuropsychiatric symptoms of dementia.medRxiv : the preprint server for health sciences · 2026
    Article
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  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
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  16. Article
  17. Review
  18. Review
  19. Therapeutic Potential ofJournal of inflammation research · 2026
    Review
  20. Article

51 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Manish KumarChitkara College of Pharmacy, Chitkara University, Punjab, India. manish.kumar@chitkara.edu.in.ORCID http://orcid.org/0000-0001-6697-544X
Nitin BansalDepartment of Pharmaceutical Sciences, Chaudhary Bansi Lal University (CBLU), Bhiwani, Haryana, 127021, India.ORCID http://orcid.org/0000-0002-2792-7469
Chaudhary Devi Lal University · INChitkara University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the foremost type of dementia that afflicts considerable morbidity and mortality in aged population. Several transcription molecules, pathways, and molecular mechanisms such as oxidative stress, inflammation, autophagy, and immune system interact in a multifaceted way that disrupt physiological processes (cell growth, differentiation, survival, lipid and energy metabolism, endocytosis) leading to apoptosis, tauopathy, β-amyloidopathy, neuron, and synapse loss, which play an important role in AD pathophysiology. Despite of stupendous advancements in pathogenic mechanisms, treatment of AD is still a nightmare in the field of medicine. There is compelling urgency to find not only symptomatic but effective disease-modifying therapies. Recently, phosphoinositide 3-kinase (PI3K) and Akt are identified as a pathway triggered by diverse stimuli, including insulin, growth factors, cytokines, and cellular stress, that link amyloid-β, neurofibrillary tangles, and brain atrophy. The present review aims to explore and analyze the role of PI3K-Akt pathway in AD and agents which may modulate Akt and have therapeutic prospects in AD. The literature was researched using keywords "PI3K-Akt" and "Alzheimer's disease" from PubMed, Web of Science, Bentham, Science Direct, Springer Nature, Scopus, and Google Scholar databases including books. Articles published from 1992 to 2021 were prioritized and analyzed for their strengths and limitations, and most appropriate ones were selected for the purpose of review. PI3K-Akt pathway regulates various biological processes such as cell proliferation, motility, growth, survival, and metabolic functions, and inhibits many neurotoxic mechanisms. Furthermore, experimental data indicate that PI3K-Akt signaling might be an important therapeutic target in treatment of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainHumansNeurofibrillary TanglesNeuronsOxidative StressPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAmyloid beta-PeptidesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAcetylcholineAmyloidInflammationNeurofibrillary tanglesNeuroprotectionOxidative stress

Identifiers

PMID34699027
OpenAlexW3211236156

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.