Evidence map›Paper›PMID 18607773›Full record

ArticleJournal of molecular neuroscience : MN2009

The genetics of Alzheimer's disease in Brazil: 10 years of analysis in a unique population.

J R M Oliveira, A L Nishimura, R R Lemos, M Zatz

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. A hypnic hypothesis of Alzheimer's disease.Neuro-degenerative diseases · 2013
    Review
  5. Protective effect of the APOE-e3 allele in Alzheimer's disease.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2012
    Article
  6. 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

4 authors at 2 institutions in 1 country.

J R M OliveiraDepartment of Neuropsychiatry, Federal University of Pernambuco, Recife, PE, Brazil. joao.ricardo@ufpe.br
A L Nishimura
R R Lemos
M Zatz
Universidade de São Paulo · BRUniversidade Federal de Pernambuco · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's Disease (AD) is the most common type of dementia among the elderly, with devastating consequences for the patient, their relatives, and caregivers. More than 300 genetic polymorphisms have been involved with AD, demonstrating that this condition is polygenic and with a complex pattern of inheritance. This paper aims to report and compare the results of AD genetics studies in case-control and familial analysis performed in Brazil since our first publication, 10 years ago. They include the following genes/markers: Apolipoprotein E (APOE), 5-hidroxytryptamine transporter length polymorphic region (5-HTTLPR), brain-derived neurotrophin factor (BDNF), monoamine oxidase A (MAO-A), and two simple-sequence tandem repeat polymorphisms (DXS1047 and D10S1423). Previously unpublished data of the interleukin-1alpha (IL-1alpha) and interleukin-1 beta (IL-1beta) genes are reported here briefly. Results from others Brazilian studies with AD patients are also reported at this short review. Four local families studied with various markers at the chromosome 21, 19, 14, and 1 are briefly reported for the first time. The importance of studying DNA samples from Brazil is highlighted because of the uniqueness of its population, which presents both intense ethnical miscegenation, mainly at the east coast, but also clusters with high inbreeding rates in rural areas at the countryside. We discuss the current stage of extending these studies using high-throughput methods of large-scale genotyping, such as single nucleotide polymorphism microarrays, associated with bioinformatics tools that allow the analysis of such extensive number of genetics variables, with different levels of penetrance. There is still a long way between the huge amount of data gathered so far and the actual application toward the full understanding of AD, but the final goal is to develop precise tools for diagnosis and prognosis, creating new strategies for better treatments based on genetic profile.

Indexed as

ConsanguinityGenetic MarkersAlzheimer DiseaseApolipoproteins EBrain-Derived Neurotrophic FactorBrazilCase-Control StudiesHumansInterleukin-1alphaInterleukin-1betaMonoamine OxidasePenetrancePolymorphism, GeneticRisk FactorsSerotonin Plasma Membrane Transport ProteinsApolipoproteins EBrain-Derived Neurotrophic FactorGenetic MarkersInterleukin-1alphaInterleukin-1betaMonoamine OxidaseSerotonin Plasma Membrane Transport ProteinsSLC6A4 protein, human

Identifiers

PMID18607773
OpenAlexW2034351739

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.