Evidence map›Paper›PMID 37186274›Full record

ReviewApoptosis : an international journal on programmed cell death2023

Apoptosis in Alzheimer's disease: insight into the signaling pathways and therapeutic avenues.

Sneha Kumari, Rishika Dhapola, Dibbanti HariKrishna Reddy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
163citing papers in PubMed, 3 pooled it
46.4field-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

163 citing papers in PubMed, 3 syntheses or guidelines pooled it, 267 citations in OpenAlex.

  1. Pooled it
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  7. Unveiling the pathogenesis and therapeutic strategies of Alzheimer's disease through cuproptosis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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  12. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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103 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

3 authors at 1 institution in 1 country.

Sneha KumariDepartment of Pharmacology, School of Health Sciences, Central University of Punjab, Ghudda, Bathinda, Punjab, 151401, India.
Rishika DhapolaDepartment of Pharmacology, School of Health Sciences, Central University of Punjab, Ghudda, Bathinda, Punjab, 151401, India.
Dibbanti HariKrishna ReddyDepartment of Pharmacology, School of Health Sciences, Central University of Punjab, Ghudda, Bathinda, Punjab, 151401, India. harikrishnareddy0011@gmail.com.
Central University of Punjab · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by the accumulation of hyperphosphorylated tau and amyloid-β (Aβ) protein resulting in synaptic loss and apoptosis. Aβ and tau deposition trigger apoptotic pathways that result in neuronal death. Apoptosis is considered to be responsible for manifestations associated with AD under pathological conditions. It regulates via extrinsic and intrinsic pathways. It activates various proteins including Bcl-2 family proteins like Bax, Bad, Bid, Bcl-XS, Bcl-XL and caspases comprising of initiator, effector and inflammatory caspases carried out through a cascade of events that finally lead to cell disintegration. The apoptotic elements interact with trophic factors, signaling molecules including Ras-ERK, JNK, GSK-3β, BDNF/TrkB/CREB and PI3K/AKT/mTOR. Ras-ERK signaling is involved in the progression of cell cycle and apoptosis. JNK pathway is also upregulated in AD which results in decreased expression of anti-apoptotic proteins. JAK-STAT triggers caspase-3 mediated apoptosis leading to neurodegeneration. The imbalance between autophagy and apoptosis is regulated by PI3K/Akt/mTOR pathway. GSK-3β is involved in the stimulation of pro-apoptotic factors resulting in dysregulation of apoptosis. Drugs like filgrastim, epigallocatechin gallate, curcumin, nicergoline and minocycline are under development which target these pathways and modulate the disease condition. This study sheds light on apoptotic pathways that are cardinal for neuronal survival and perform crucial role in the occurrence of AD along with the trends in therapeutics targeting apoptosis induced AD. To develop prospective treatments for AD, it is desirable to elucidate potential targets including restoration apoptotic balance, regulation of caspases, Bcl-2 and other crucial proteins involved in apoptosis mediated AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesApoptosisCaspasesGlycogen Synthase Kinase 3 betaHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Signal TransductionTOR Serine-Threonine KinasesAmyloid beta-PeptidesCaspasesGlycogen Synthase Kinase 3 betaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2TOR Serine-Threonine KinasesAlzheimer's diseaseApoptosisBcl-2CaspaseDrugs

Identifiers

PMID37186274
OpenAlexW4366976470

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.