Evidence map›Paper›PMID 40300834›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2025

The Role of Neprilysin and Insulin-Degrading Enzyme in the Etiology of Sporadic Alzheimer's Disease.

Takahiro Morito, Shoko Hashimoto, Risa Takamura, Naoto Watamura, Naomasa Kakiya, Ryo Fujioka, Naomi Mihara, Misaki Sekiguchi, Kaori Watanabe-Iwata, Naoko Kamano and 7 more

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Increased Amyloidogenic Neuronal Injury in HIV-1-infected APP-KI Alzheimer's disease mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  5. Review
  6. Review
  7. Review
  8. 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

17 authors.

Takahiro MoritoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan takahiro.morito@riken.jp takaomi.saido@riken.jp.
Shoko HashimotoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Risa TakamuraLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Naoto WatamuraLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Naomasa KakiyaLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Ryo FujiokaLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Naomi MiharaLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Misaki SekiguchiLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Kaori Watanabe-IwataDepartment of Genome-based Drug Discovery & Unit for Brain Research, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8521, Japan.
Naoko KamanoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Mohan QiLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Yukio MatsubaLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Satoshi TsubukiLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Takashi SaitoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Nobuhisa IwataDepartment of Genome-based Drug Discovery & Unit for Brain Research, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8521, Japan.ORCID 0000-0001-8721-7947
Hiroki SasaguriLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Takaomi C SaidoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan takahiro.morito@riken.jp takaomi.saido@riken.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An age-dependent decline in the amyloid-β (Aβ)-degrading enzyme neprilysin (NEP) has been implicated in the pathogenesis of sporadic Alzheimer's disease (AD). Recently identified risk alleles in the NEP-coding gene further support its role in AD etiology. However, evidence for the impact of NEP on the pathophysiological progression of Aβ plaque formation, particularly in comparison with another Aβ-degrading enzyme, insulin-degrading enzyme (IDE), is still lacking. Furthermore, the functional impact of the NEP mutation, M8V, caused by the AD risk allele in the NEP gene, remains unexplored. Here we found that NEP deficiency in

Indexed as

Alzheimer DiseaseInsulysinNeprilysinAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsCell Line, TumorFemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMutationPlaque, AmyloidAmyloid beta-PeptidesAmyloid beta-Protein PrecursorInsulysinNeprilysinAbetaAlzheimerdegradationGWASmutationneprilysin

Identifiers

PMID40300834
PMCPMC12139590

What Socratic 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 Socratic graph.