Evidence map›Paper›PMID 29224179›Full record

ArticleMolecular neurobiology2018

Antidiabetic Polypill Improves Central Pathology and Cognitive Impairment in a Mixed Model of Alzheimer's Disease and Type 2 Diabetes.

Carmen Infante-Garcia, Juan Jose Ramos-Rodriguez, Carmen Hierro-Bujalance, Esperanza Ortegon, Eleanor Pickett, Rosemary Jackson, Fernando Hernandez-Pacho, Tara Spires-Jones, Monica Garcia-Alloza

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Article
  6. Review
  7. Review
  8. Antidiabetic Drugs in the Treatment of Alzheimer's Disease.International journal of molecular sciences · 2022
    Review
  9. Review
  10. Article
  11. Effects of classical PKC activation on hippocampal neurogenesis and cognitive performance: mechanism of action.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  12. Article
  13. Antiaging Therapies, Cognitive Impairment, and Dementia.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020
    Review
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  15. Article
  16. Article
  17. Article
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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

9 authors at 3 institutions in 2 countries.

Carmen Infante-GarciaDivision of Physiology, School of Medicine, Instituto de Investigación e Innovación en Ciencias Biomedicas de la Provincia de Cadiz (INIBICA), Universidad de Cadiz, Plaza Fragela sn, 4 piso 410, Cadiz, Spain.
Juan Jose Ramos-RodriguezDivision of Physiology, School of Medicine, Instituto de Investigación e Innovación en Ciencias Biomedicas de la Provincia de Cadiz (INIBICA), Universidad de Cadiz, Plaza Fragela sn, 4 piso 410, Cadiz, Spain.
Carmen Hierro-BujalanceDivision of Physiology, School of Medicine, Instituto de Investigación e Innovación en Ciencias Biomedicas de la Provincia de Cadiz (INIBICA), Universidad de Cadiz, Plaza Fragela sn, 4 piso 410, Cadiz, Spain.
Esperanza OrtegonDivision of Physiology, School of Medicine, Instituto de Investigación e Innovación en Ciencias Biomedicas de la Provincia de Cadiz (INIBICA), Universidad de Cadiz, Plaza Fragela sn, 4 piso 410, Cadiz, Spain.
Eleanor PickettUK Dementia Research Institute, Centre for Discovery Brain Sciences, Edinburgh Neuroscience, and Centre for Dementia Prevention, The University of Edinburgh, Edinburgh, UK.
Rosemary JacksonUK Dementia Research Institute, Centre for Discovery Brain Sciences, Edinburgh Neuroscience, and Centre for Dementia Prevention, The University of Edinburgh, Edinburgh, UK.
Fernando Hernandez-PachoClinical Management Unit of Laboratories, Hospital Universitario Puerta del Mar, Cadiz, Spain.
Tara Spires-JonesUK Dementia Research Institute, Centre for Discovery Brain Sciences, Edinburgh Neuroscience, and Centre for Dementia Prevention, The University of Edinburgh, Edinburgh, UK.
Monica Garcia-AllozaDivision of Physiology, School of Medicine, Instituto de Investigación e Innovación en Ciencias Biomedicas de la Provincia de Cadiz (INIBICA), Universidad de Cadiz, Plaza Fragela sn, 4 piso 410, Cadiz, Spain. monica.garcia@uca.es.ORCID http://orcid.org/0000-0003-1610-4114
Universidad de Cádiz · ESUK Dementia Research Institute · GBHospital Universitario Puerta del Mar · ES

Funding

European Research Council (ALZSYN)Fundación Eugenio Rodríguez Pascual (ES) (2015)Ministerio de Educación, Cultura y Deporte en el marco del Programa Estatal de Promoción del Talento y su Empleabilidad en I+D+i, Subprograma Estatal de Movilidad, del Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016. PRX16/00246National Programme for Research Aimed at the Challenges of Society, financed by the Agencia Estatal de Investigación (AEI) and the Fondo Europeo de Desarrollo Regional (FEDER). BFU 2016-75038-RProyectos de Excelencia, Consejería de Economía, Innovación, Ciencia y Empleo Junta de Andalucía . (P11-CTS-7847)
6 · The paper itself

Abstract

Type 2 diabetes (T2D) is an important risk factor to suffer dementia, being Alzheimer's disease (AD) as the most common form. Both AD and T2D are closely related to aging and with a growing elderly population it might be of relevance to explore new therapeutic approaches that may slow or prevent central complications associated with metabolic disorders. Therefore, we propose the use of the antidiabetic polypill (PP), a pharmacological cocktail, commonly used by T2D patients that include metformin, aspirin, simvastatin, and an angiotensin-converting enzyme inhibitor. In order to test the effects of PP at the central level, we have long-term treated a new mixed model of AD-T2D, the APP/PS1xdb/db mouse. We have analyzed AD pathological features and the underlying specific characteristics that relate AD and T2D. As expected, metabolic alterations were ameliorated after PP treatment in diabetic mice, supporting a role for PP in maintaining pancreatic activity. At central level, PP reduced T2D-associated brain atrophy, showing both neuronal and synaptic preservation. Tau and amyloid pathologies were also reduced after PP treatment. Furthermore, we observed a reduction of spontaneous central bleeding and inflammation after PP treatment in diabetic mice. As consequence, learning and memory processes were improved after PP treatment in AD, T2D, and AD-T2D mice. Our data provide the basis to further analyze the role of PP, as an alternative or adjuvant, to slow down or delay the central complications associated with T2D and AD.

Indexed as

PolypharmacyAlzheimer DiseaseAmyloidAmyloid beta-PeptidesAnimalsAtrophyBrainCerebral HemorrhageCognitive DysfunctionDiabetes Mellitus, Type 2Disease Models, AnimalHumansHypoglycemic AgentsInflammationLipidsMice, TransgenicAmyloidAmyloid beta-PeptidesHypoglycemic AgentsLipidstau ProteinsAlzheimer’s diseaseAmyloid-betaHemorrhageInflammationPolypillTauType 2 diabetes

Identifiers

PMID29224179
OpenAlexW2775361101

What OpenQuestion holds

Textmetadata
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.