Evidence map›Paper›PMID 15181243›Full record

ReviewJournal of molecular neuroscience : MN2004

Apolipoprotein E4 as a target for developing new therapeutics for Alzheimer's disease.

Lorenzo M Refolo, Howard M Fillit

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular neuroscience : MN, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

7 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Direct Transcriptional Effects of Apolipoprotein E.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  4. Review
  5. Review
  6. Review
  7. 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

2 authors at 1 institution in 2 countries.

Lorenzo M RefoloInstitute for the Study of Aging, New York, NY 10153, USA. lrefolo@aging-institute.org
Howard M Fillit
Institute on Aging · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The identification of factors that influence the onset or progression of the sporadic form of Alzheimer's disease (AD) is a key step toward understanding its mechanism(s) and developing successful rational therapies. The apoE genotype has been identified as a powerful risk factor for AD that may account for as much as 50% of the sporadic form of the disease. As the major risk factor for late-onset AD, apolipoprotein E4 (apoE4) should be considered a good target for AD drug discovery. However, despite knowing for over a decade that apoE4 is detrimental to the disease process, we still remain uncertain about the molecular mechanisms subserving the risk-factor activity of apoE4. This, coupled with the fact that we know relatively little about the function(s) of apoE in brain, has presented a barrier to developing apoE-based therapeutics for AD. Progress has been made in understanding the neurobiology of apoE; a number of potentially overlapping functions have been ascribed, which include lipid transport, neuronal repair, dendritic growth, maintenance of synaptic plasticity, and anti-inflammatory activities. Until the gaps are filled in our understanding of the pathogenic function(s) of apoE4, therapeutic strategies targeting this protein will lag behind the development of other AD therapies. Putative pathological functions, or risk-factor activities, of apoE4 include its role in beta-amyloid deposition, neurofibrillary tangle formation, synaptic loss, lipid dysfunction, neuroinflammation, and oxidative stress.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesApolipoprotein E4Apolipoproteins EGenotypeHumansProtein IsoformsRisk FactorsAmyloid beta-PeptidesApolipoprotein E4Apolipoproteins EProtein Isoforms

Identifiers

PMID15181243
OpenAlexW2049433226

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.