Evidence map›Paper›PMID 36591205›Full record

ReviewACS omega2022

Preclinical Models for Alzheimer's Disease: Past, Present, and Future Approaches.

Ansab Akhtar, Shraddha M Gupta, Shubham Dwivedi, Devendra Kumar, Mohd Farooq Shaikh, Arvind Negi

Open access · goldAbstract readReview
In one paragraph

Review in ACS omega, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 3 pooled it
7.2field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 3 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Efficacy of reminiscence therapy in improving cognitive decline: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Pooled it
  3. The Role of Hydrogen Sulfide (HInternational journal of molecular sciences · 2023
    Pooled it
  4. Review
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  10. Review
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  12. Neuroprotective Effect of the Combined Extract ofInternational journal of molecular sciences · 2026
    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

6 authors at 4 institutions in 3 countries.

Ansab AkhtarDepartment of Pharmaceutical Sciences, School of Health Sciences and Technology, UPES, Dehradun, Uttarakhand, Dehradun 248007, India.ORCID https://orcid.org/0000-0002-4839-4454
Shraddha M GuptaDepartment of Pharmaceutical Sciences, School of Health Sciences and Technology, UPES, Dehradun, Uttarakhand, Dehradun 248007, India.ORCID https://orcid.org/0000-0002-8931-4713
Shubham DwivediDepartment of Pharmaceutical Sciences, School of Health Sciences and Technology, UPES, Dehradun, Uttarakhand, Dehradun 248007, India.
Devendra KumarFaculty of Pharmacy, DIT University, Uttarakhand, Dehradun 248009, India.
Mohd Farooq ShaikhNeuropharmacology Research Strength, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Bandar Sunway, Selangor 47500, Malaysia.ORCID https://orcid.org/0000-0001-9865-6224
Arvind NegiDepartment of Bioproducts and Biosystems, Aalto University, FI-00076 Espoo, Finland.ORCID https://orcid.org/0000-0002-0341-9291
University of Petroleum and Energy Studies · INAalto University · FIDehradun Institute of Technology University · INMonash University Malaysia · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A robust preclinical disease model is a primary requirement to understand the underlying mechanisms, signaling pathways, and drug screening for human diseases. Although various preclinical models are available for several diseases, clinical models for Alzheimer's disease (AD) remain underdeveloped and inaccurate. The pathophysiology of AD mainly includes the presence of amyloid plaques and neurofibrillary tangles (NFT). Furthermore, neuroinflammation and free radical generation also contribute to AD. Currently, there is a wide gap in scientific approaches to preventing AD progression. Most of the available drugs are limited to symptomatic relief and improve deteriorating cognitive functions. To mimic the pathogenesis of human AD, animal models like 3XTg-AD and 5XFAD are the primarily used mice models in AD therapeutics. Animal models for AD include intracerebroventricular-streptozotocin (ICV-STZ), amyloid beta-induced, colchicine-induced, etc., focusing on parameters such as cognitive decline and dementia. Unfortunately, the translational rate of the potential drug candidates in clinical trials is poor due to limitations in imitating human AD pathology in animal models. Therefore, the available preclinical models possess a gap in AD modeling. This paper presents an outline that critically assesses the applicability and limitations of the current approaches in disease modeling for AD. Also, we attempted to provide key suggestions for the best-fit model to evaluate potential therapies, which might improve therapy translation from preclinical studies to patients with AD.

Identifiers

PMID36591205
PMCPMC9798399
OpenAlexW4311311270

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.