Evidence map›Paper›PMID 23028126›Full record

ReviewCold Spring Harbor perspectives in medicine2012

The genetics of Alzheimer disease.

Rudolph E Tanzi

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 437 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
437citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

437 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  5. Trial
  6. Synaptic Proteostasis in Health and Disease.Journal of neurochemistry · 2026
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377 more citing papers are in PubMed but not listed here.

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

1 author.

Rudolph E TanziGenetics and Aging Research Unit, Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02129, USA. tanzi@helix.mgh.harvard.edu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Family history is the second strongest risk factor for Alzheimer disease (AD) following advanced age. Twin and family studies indicate that genetic factors are estimated to play a role in at least 80% of AD cases. The inheritance of AD exhibits a dichotomous pattern. On one hand, rare mutations in APP, PSEN1, and PSEN2 virtually guarantee early-onset (<60 years) familial AD, which represents ∼5% of AD. On the other hand, common gene polymorphisms, such as the ε4 and ε2 variants of the APOE gene, can influence susceptibility for ∼50% of the common late-onset AD. These four genes account for 30%-50% of the inheritability of AD. Genome-wide association studies have recently led to the identification of 11 additional AD candidate genes. This paper reviews the past, present, and future attempts to elucidate the complex and heterogeneous genetic underpinnings of AD.

Indexed as

ADAM10 ProteinADAM ProteinsAge of OnsetAlzheimer DiseaseAmyloid Precursor Protein SecretasesApolipoproteins EGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMembrane ProteinsMutationPolymorphism, GeneticRisk FactorsADAM10 ProteinADAM10 protein, humanADAM ProteinsAmyloid Precursor Protein SecretasesApolipoproteins EMembrane Proteins

Identifiers

PMID23028126
PMCPMC3475404

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.