Evidence map›Paper›PMID 34852746›Full record

ReviewCurrent neuropharmacology2022

BACE1: A Key Regulator in Alzheimer's Disease Progression and Current Development of its Inhibitors.

Smith Patel, Ankush Vardhaman Bansoad, Rakesh Singh, Gopal L Khatik

Open access · greenAbstract readReview
In one paragraph

Review in Current neuropharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Effects of BACE2 polymorphisms on verbal memory in the general population.European archives of psychiatry and clinical neuroscience · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. The Clinical Trials Landscape for Alzheimer's Disease.CNS neuroscience & therapeutics · 2025
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review
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

4 authors at 1 institution in 1 country.

Smith PatelDepartment of Medicinal Chemistry, National Institute of Pharmaceutical Education and Research-Raebareli, New Transit Campus, Bijnor-Sisendi Road, Sarojini Nagar, Near CRPF Base Camp, Lucknow (Uttar Pradesh), 226002, India.
Ankush Vardhaman BansoadDepartment of Pharmacology & Toxicology, National Institute of Pharmaceutical Education and Research-Raebareli, New Transit Campus, Bijnor-Sisendi Road, Sarojini Nagar, Near CRPF Base Camp, Lucknow (Uttar Pradesh), 226002, India.
Rakesh SinghDepartment of Pharmacology & Toxicology, National Institute of Pharmaceutical Education and Research-Raebareli, New Transit Campus, Bijnor-Sisendi Road, Sarojini Nagar, Near CRPF Base Camp, Lucknow (Uttar Pradesh), 226002, India.
Gopal L KhatikDepartment of Medicinal Chemistry, National Institute of Pharmaceutical Education and Research-Raebareli, New Transit Campus, Bijnor-Sisendi Road, Sarojini Nagar, Near CRPF Base Camp, Lucknow (Uttar Pradesh), 226002, India.
National Institute of Pharmaceutical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is a chronic neurodegenerative disease with no specific disease-modifying treatment. β-secretase (BACE1) is considered the potential and rationale target because it is involved in the rate-limiting step, which produces toxic Aβ

objectiveThis study aims to discuss the role and implications of BACE1 and its inhibitors in the management of AD.

methodsWe have searched and collected the relevant quality work from PubMed using the following keywords "BACE1", BACE2", "inhibitors", and "Alzheimer's disease". In addition, we included the work which discusses the role of BACE1 in AD and the recent work on its inhibitors.

resultsIn this review, we have discussed the importance of BACE1 in regulating AD progression and the current development of BACE1 inhibitors. However, the development of a BACE1 inhibitor is very challenging due to the large active site of BACE1. Nevertheless, some of the BACE1 inhibitors have managed to enter advanced phases of clinical trials, such as MK-8931 (Verubecestat), E2609 (Elenbecestat), AZD3293 (Lanabecestat), and JNJ-54861911 (Atabecestat). This review also sheds light on the prospect of BACE1 inhibitors as the most effective therapeutic approach in delaying or preventing AD progression.

conclusionBACE1 is involved in the progression of AD. The current ongoing or failed clinical trials may help understand the role of BACE1 inhibition in regulating the Aβ load and cognitive status of AD patients.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesDisease ProgressionHumansAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBACE1 protein, humanAlzheimer’s diseaseAβ42 peptideBACE1Beta-secretaseinhibitorsneurodegenerative disease

Identifiers

PMID34852746
PMCPMC9886827
OpenAlexW3217747820

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.