Evidence map›Paper›PMID 27863488›Full record

ArticleBMC systems biology2016

Mathematical model on Alzheimer's disease.

Wenrui Hao, Avner Friedman

Open access · diamondAbstract read
In one paragraph

Article in BMC systems biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.3field-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

57 citing papers in PubMed, 152 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Mathematical Modeling of Neuroinflammation in Neurodegenerative Diseases.CPT: pharmacometrics & systems pharmacology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. The role of IPFrontiers in computational neuroscience · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 at 2 institutions in 1 country.

Wenrui HaoDepartment of Mathematics, The Penn State University, University Park, 16802, PA, USA. hao.50@mbi.osu.edu.
Avner FriedmanMathematical Biosciences Institute & Department of Mathematics, The Ohio State University, Columbus, 43210, OH, USA.
Pennsylvania State University · USThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer disease (AD) is a progressive neurodegenerative disease that destroys memory and cognitive skills. AD is characterized by the presence of two types of neuropathological hallmarks: extracellular plaques consisting of amyloid β-peptides and intracellular neurofibrillary tangles of hyperphosphorylated tau proteins. The disease affects 5 million people in the United States and 44 million world-wide. Currently there is no drug that can cure, stop or even slow the progression of the disease. If no cure is found, by 2050 the number of alzheimer's patients in the U.S. will reach 15 million and the cost of caring for them will exceed $ 1 trillion annually.

resultsThe present paper develops a mathematical model of AD that includes neurons, astrocytes, microglias and peripheral macrophages, as well as amyloid β aggregation and hyperphosphorylated tau proteins. The model is represented by a system of partial differential equations. The model is used to simulate the effect of drugs that either failed in clinical trials, or are currently in clinical trials.

conclusionsBased on these simulations it is suggested that combined therapy with TNF- α inhibitor and anti amyloid β could yield significant efficacy in slowing the progression of AD.

Indexed as

Models, BiologicalAlzheimer DiseaseAmyloid beta-PeptidesAstrocytesChemokine CCL2Disease ProgressionHumansMacrophagesMicrogliaNeuronsPhosphorylationProtein AggregatesProtein MultimerizationProtein Structure, Secondarytau ProteinsTransforming Growth Factor betaAmyloid beta-PeptidesCCL2 protein, humanChemokine CCL2Protein Aggregatestau ProteinsTransforming Growth Factor betaTumor Necrosis Factor-alphaAlzheimer diseaseDrug treatmentMathematical modeling

Identifiers

PMID27863488
PMCPMC5116206
OpenAlexW2552032209

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.