Evidence map›Paper›PMID 26556341›Full record

ReviewInternational journal of molecular sciences2015

Alzheimer's Disease: Mechanism and Approach to Cell Therapy.

Takashi Amemori, Pavla Jendelova, Jiri Ruzicka, Lucia Machova Urdzikova, Eva Sykova

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 3 pooled it
7.2field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Probiotic supplementation improved cognitive function in cognitively impaired and healthy older adults: a systematic review of recent trials.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Alzheimer's Disease Association with Metals and Metalloids Concentration in Blood and Urine.International journal of environmental research and public health · 2022
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Pharmaceutical biology · 2020
    Review
  19. Article
  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

5 authors at 1 institution in 1 country.

Takashi AmemoriDepartment of Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic. amemori@biomed.cas.cz.
Pavla JendelovaDepartment of Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic. jendel@biomed.cas.cz.
Jiri RuzickaDepartment of Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic. j.ruzicka@biomed.cas.cz.
Lucia Machova UrdzikovaDepartment of Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic. urdzikl@biomed.cas.cz.
Eva SykovaDepartment of Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic. sykova@biomed.cas.cz.
Czech Academy of Sciences · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common form of dementia. The risk of AD increases with age. Although two of the main pathological features of AD, amyloid plaques and neurofibrillary tangles, were already recognized by Alois Alzheimer at the beginning of the 20th century, the pathogenesis of the disease remains unsettled. Therapeutic approaches targeting plaques or tangles have not yet resulted in satisfactory improvements in AD treatment. This may, in part, be due to early-onset and late-onset AD pathogenesis being underpinned by different mechanisms. Most animal models of AD are generated from gene mutations involved in early onset familial AD, accounting for only 1% of all cases, which may consequently complicate our understanding of AD mechanisms. In this article, the authors discuss the pathogenesis of AD according to the two main neuropathologies, including senescence-related mechanisms and possible treatments using stem cells, namely mesenchymal and neural stem cells.

Indexed as

Cell- and Tissue-Based TherapyAge of OnsetAgingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsDisease Models, AnimalEnergy MetabolismHumansImmunotherapyMutationNeurogliaPlaque, AmyloidStem CellsStem Cell Transplantationtau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer’s diseaseamyloid-βmesenchymal stem cellsneural stem cellsTau

Identifiers

PMID26556341
PMCPMC4661820
OpenAlexW1901837091

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.