Evidence map›Paper›PMID 34940364›Full record

ReviewBioengineering (Basel, Switzerland)2021

Alzheimer's Disease: Current Perspectives and Advances in Physiological Modeling.

E Josephine Boder, Ipsita A Banerjee

Abstract readReview
In one paragraph

Review in Bioengineering (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Accelerated neuronal agingFrontiers in aging neuroscience · 2022
    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

2 authors.

E Josephine BoderDepartment of Chemistry, Fordham University, 441 E. Fordham Road, Bronx, NY 10458, USA.ORCID 0000-0003-4631-2280
Ipsita A BanerjeeDepartment of Chemistry, Fordham University, 441 E. Fordham Road, Bronx, NY 10458, USA.

Funding

Fordham University Internal Research Grant
6 · The paper itself

Abstract

Though Alzheimer's disease (AD) is the most common cause of dementia, complete disease-modifying treatments are yet to be fully attained. Until recently, transgenic mice constituted most in vitro model systems of AD used for preclinical drug screening; however, these models have so far failed to adequately replicate the disease's pathophysiology. However, the generation of humanized APOE4 mouse models has led to key discoveries. Recent advances in stem cell differentiation techniques and the development of induced pluripotent stem cells (iPSCs) have facilitated the development of novel in vitro devices. These "microphysiological" systems-in vitro human cell culture systems designed to replicate in vivo physiology-employ varying levels of biomimicry and engineering control. Spheroid-based organoids, 3D cell culture systems, and microfluidic devices or a combination of these have the potential to replicate AD pathophysiology and pathogenesis in vitro and thus serve as both tools for testing therapeutics and models for experimental manipulation.

Indexed as

Alzheimer’s diseasebiomimeticsmicrophysiological systemsneurodegenerative diseases

Identifiers

PMID34940364
PMCPMC8698996

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.