Evidence map›Paper›PMID 20382260›Full record

ReviewBiochimica et biophysica acta2010

Isoprenoids, small GTPases and Alzheimer's disease.

Gero P Hooff, W Gibson Wood, Walter E Müller, Gunter P Eckert

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.1field-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

58 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. CoQAntioxidants (Basel, Switzerland) · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. The role of statins in lung cancer.Archives of medical science : AMS · 2022
    Article
  12. Metabolic reprogramming of pulmonary fibrosis.Frontiers in pharmacology · 2022
    Review
  13. Article
  14. Metabolic disorder in Alzheimer's disease.Metabolic brain disease · 2021
    Review
  15. Article
  16. Article
  17. Inhibition of the mevalonate pathway improves myocardial fibrosis.Experimental and therapeutic medicine · 2021
    Article
  18. SOAT1 promotes mevalonate pathway dependency in pancreatic cancer.The Journal of experimental medicine · 2020
    Article
  19. Review
  20. Lipids and Alzheimer's Disease.International journal of molecular sciences · 2020
    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

4 authors at 2 institutions in 2 countries.

Gero P HooffDepartment of Pharmacology, Campus Riedberg, Goethe University, 60438 Frankfurt, Germany.
W Gibson Wood
Walter E Müller
Gunter P Eckert
Goethe University Frankfurt · DEGeriatric Research Education and Clinical Center · US

Funding

PATHOGENESIS OF PHOSPHOLIPASES A2 IN ADP01AG018357 · NIA · UNIVERSITY OF MISSOURI-COLUMBIA · PI SUN, GRACE Y · 2001 to 2012
$10.4M
Amyloid Beta-Protein: ApoE and Cholesterol HomeostasisR01AG023524 · NIA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WOOD, WELLINGTON GIBSON · 2005 to 2009
$1.2M
NIA NIH HHS AG18357NIA NIH HHS AG23524NIA NIH HHS P01 AG018357NIA NIH HHS R01 AG023524
6 · The paper itself

Abstract

The mevalonate pathway is a crucial metabolic pathway for most eukaryotic cells. Cholesterol is a highly recognized product of this pathway but growing interest is being given to the synthesis and functions of isoprenoids. Isoprenoids are a complex class of biologically active lipids including for example, dolichol, ubiquinone, farnesylpyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP). Early work had shown that the long-chain isoprenoid dolichol is decreased but that dolichyl phosphate and ubiquinone are elevated in brains of Alzheimer's disease (AD) patients. Until recently, levels of their biological active precursors FPP and GGPP were unknown. These short-chain isoprenoids are critical in the post-translational modification of certain proteins which function as molecular switches in numerous signaling pathways. The major protein families belong to the superfamily of small GTPases, consisting of roughly 150 members. Recent experimental evidence indicated that members of the small GTPases are involved in AD pathogenesis and stimulated interest in the role of FPP and GGPP in protein prenylation and cell function. A straightforward prediction derived from those studies was that FPP and GGPP levels would be elevated in AD brains as compared with normal neurological controls. For the first time, recent evidence shows significantly elevated levels of FPP and GGPP in human AD brain tissue. Cholesterol levels did not differ between AD and control samples. One obvious conclusion is that homeostasis of FPP and GGPP but not of cholesterol is specifically targeted in AD. Since prenylation of small GTPases by FPP or GGPP is indispensable for their proper function we are proposing that these two isoprenoids are up-regulated in AD resulting in an over abundance of certain prenylated proteins which contributes to neuronal dysfunction.

Indexed as

AgingAlzheimer DiseaseAnimalsCholesterolHumansMetabolic Networks and PathwaysMevalonic AcidModels, BiologicalMonomeric GTP-Binding ProteinsNerve DegenerationProtein PrenylationTerpenesCholesterolMevalonic AcidMonomeric GTP-Binding ProteinsTerpenes

Identifiers

PMID20382260
PMCPMC2886181
OpenAlexW2013382634

What OpenQuestion holds

Textmetadata
LicenceTDM
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.