Evidence map›Paper›PMID 22695623›Full record

ReviewJournal of Alzheimer's disease : JAD2013

Characterizing the preclinical stages of Alzheimer's disease and the prospect of presymptomatic intervention.

Richard J Caselli, Eric M Reiman

Abstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
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  7. Nanomedicine: A New Frontier in Alzheimer's Disease Drug Targeting.Central nervous system agents in medicinal chemistry · 2025
    Review
  8. Article
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  10. Review
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  13. Article
  14. PSEN2 and ABCA7 variants causing early-onset preclinical pathological changes in Alzheimer's disease: a case report and literature review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
    Review
  15. Article
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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 2 institutions in 1 country.

Richard J CaselliDepartment of Neurology, Mayo Clinic Phoenix, AZ 85259, USA. caselli.richard@mayo.edu
Eric M Reiman
Mayo Clinic Hospital · USUniversity of Arizona · US

Funding

Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI GONZALEZ HERNANDEZ, GRACIELA · 2001 to 2020
$32.5M
PET, APOE & the Preclinical Course of Alzheimer's DiseaseR01AG031581 · NIA · BANNER ALZHEIMER'S INSTITUTE · PI CASELLI, RICHARD J., REIMAN, ERIC MICHAEL · 2008 to 2018
$16.6M
NIA NIH HHS P30 AG019610NIA NIH HHS P30AG19610NIA NIH HHS R01 AG031581NIA NIH HHS R01AG031581
6 · The paper itself

Abstract

Studies of asymptomatic carriers of genes that are known to predispose to Alzheimer's disease (AD) have facilitated the characterization of preclinical AD. The most prevalent genetic risk factor is the ε4 allele of apolipoprotein E (APOE). Neuropathological studies of young deceased ε4 carriers have shown modest but abnormal amounts of neocortical amyloid and medial temporal neurofibrillary tangles that is also reflected in cerebrospinal fluid (CSF) biomarkers, amyloid-β, and phospho-tau in particular. MRI studies have shown progressive hippocampal and gray matter atrophy with the advent of mild cognitive impairment (MCI), and fluorodeoxyglucose PET scans show reduced cerebral metabolism in posterior cingulate and related AD regions evident even in 30 year olds. Cerebral amyloidosis disclosed by more recent amyloid ligand PET studies in asymptomatic 60 year olds increases in parallel with ε4 gene dose. Longitudinal neuropsychological studies have revealed accelerated memory decline in ε4 carriers beginning around age 55-60 years whose severity again parallels ε4 gene dose. The clinico-pathological correlation of declining memory and AD-like neuropathological change defines preclinical AD and has set the stage for the accelerated evaluation of presymptomatic AD treatments. In this article, we briefly consider some of the earliest detectable changes associated with the predisposition to AD, and some of the prevention trial strategies that have been proposed to help find treatments to reduce the risk, postpone the onset of, or completely prevent AD symptoms as soon as possible.

Indexed as

Prodromal SymptomsAgingAlzheimer DiseaseApolipoproteins EAtrophyBrainCognitive DysfunctionEarly DiagnosisHumansApolipoproteins E

Identifiers

PMID22695623
PMCPMC3628721
OpenAlexW1746965720

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.