Evidence map›Paper›PMID 34913091›Full record

ArticleCellular and molecular life sciences : CMLS2021

Long-term caffeine treatment of Alzheimer mouse models ameliorates behavioural deficits and neuron loss and promotes cellular and molecular markers of neurogenesis.

Martina Stazi, Sandra Lehmann, M Sadman Sakib, Tonatiuh Pena-Centeno, Luca Büschgens, Andre Fischer, Sascha Weggen, Oliver Wirths

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.7field-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

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Nutrition: A non-negligible factor in the pathogenesis and treatment of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Dynamic Regulation of Mitochondrial [CaInternational journal of molecular sciences · 2022
    Article
  17. Article
  18. A novelHorticulture research · 2022
    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

8 authors at 3 institutions in 1 country.

Martina StaziDepartment of Psychiatry and Psychotherapy, University Medical Center (UMG), Georg-August-University, Von-Siebold-Str. 5, 37075, Göttingen, Germany.
Sandra LehmannDepartment of Neuropathology, Heinrich-Heine-University, Düsseldorf, Germany.
M Sadman SakibGerman Center for Neurodegenerative Diseases (DZNE), Göttingen, Germany.
Tonatiuh Pena-CentenoGerman Center for Neurodegenerative Diseases (DZNE), Göttingen, Germany.
Luca BüschgensDepartment of Psychiatry and Psychotherapy, University Medical Center (UMG), Georg-August-University, Von-Siebold-Str. 5, 37075, Göttingen, Germany.
Andre FischerDepartment of Psychiatry and Psychotherapy, University Medical Center (UMG), Georg-August-University, Von-Siebold-Str. 5, 37075, Göttingen, Germany.
Sascha WeggenDepartment of Neuropathology, Heinrich-Heine-University, Düsseldorf, Germany.
Oliver WirthsDepartment of Psychiatry and Psychotherapy, University Medical Center (UMG), Georg-August-University, Von-Siebold-Str. 5, 37075, Göttingen, Germany. owirths@gwdg.de.ORCID http://orcid.org/0000-0002-4115-0334
German Center for Neurodegenerative Diseases · DEUniversity of Göttingen · DEHeinrich Heine University Düsseldorf · DE

Funding

Alzheimer Forschung Initiative 20021Deutsche Forschungsgemeinschaft WI 3472/10-1
6 · The paper itself

Abstract

Epidemiological studies indicate that the consumption of caffeine, the most commonly ingested psychoactive substance found in coffee, tea or soft drinks, reduces the risk of developing Alzheimer's disease (AD). Previous treatment studies with transgenic AD mouse models reported a reduced amyloid plaque load and an amelioration of behavioral deficits. It has been further shown that moderate doses of caffeine have the potential to attenuate the health burden in preclinical mouse models of a variety of brain disorders (reviewed in Cunha in J Neurochem 139:1019-1055, 2016). In the current study, we assessed whether long-term caffeine consumption affected hippocampal neuron loss and associated behavioral deficits in the Tg4-42 mouse model of AD. Treatment over a 4-month period reduced hippocampal neuron loss, rescued learning and memory deficits, and ameliorated impaired neurogenesis. Neuron-specific RNA sequencing analysis in the hippocampus revealed an altered expression profile distinguished by the up-regulation of genes linked to synaptic function and processes, and to neural progenitor proliferation. Treatment of 5xFAD mice, which develop prominent amyloid pathology, with the same paradigm also rescued behavioral deficits but did not affect extracellular amyloid-β (Aβ) levels or amyloid precursor protein (APP) processing. These findings challenge previous assumptions that caffeine is anti-amyloidogenic and indicate that the promotion of neurogenesis might play a role in its beneficial effects.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBiomarkersCaffeineCells, CulturedFemaleMaleMiceMice, Inbred C57BLNeurogenesisNeuronsPlaque, AmyloidAmyloid beta-PeptidesBiomarkersCaffeine5xFADAlzheimer’s diseaseAmyloidBehaviorCaffeineNeurogenesisRNA sequencingTg4-42TranscriptomeTransgenic mice

Identifiers

PMID34913091
PMCPMC8738505
OpenAlexW4200446690

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.