Evidence map›Paper›PMID 22108203›Full record

ReviewBiochimica et biophysica acta2012

PET amyloid-beta imaging in preclinical Alzheimer's disease.

Andrei G Vlassenko, Tammie L S Benzinger, John C Morris

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 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

87 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Β-Amyloid Burden is Not Associated with Cognitive Impairment in Schizophrenia: A Systematic Review.The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry · 2016
    Pooled it
  2. Article
  3. Review
  4. Preclinical evaluation of [EJNMMI research · 2026
    Article
  5. In-depth multimodal validation ofExperimental & molecular medicine · 2026
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. The AHA/ASA and DSM-V diagnostic criteria for vascular cognitive impairment identify cases with predominant vascular pathology.International journal of stroke : official journal of the International Stroke Society · 2024
    Article
  14. Article
  15. Article
  16. CoQAntioxidants (Basel, Switzerland) · 2024
    Review
  17. Article
  18. The Role of Clinical Assessment in the Era of Biomarkers.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  19. Article
  20. Review

27 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

3 authors.

Andrei G VlassenkoDepartment of Radiology, Washington University School of Medicine, St. Louis, MO, USA.
Tammie L S Benzinger
John C Morris

Funding

Smartphone-Based "Burst" Cognitive AssessmentsP01AG003991 · NIA · WASHINGTON UNIVERSITY · PI JOHN MORRIS · 1985 to 2026
$69.5M
WASHINGTON UNIVERSITY ALZHEIMERS DISEASE RESEARCH CENTERP50AG005681 · NIA · WASHINGTON UNIVERSITY · PI FAGAN, ANNE · 1985 to 2019
$52.1M
The natural history of AB accumulation in preclinical ADP01AG026276 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 2005 to 2025
$49.5M
NIA NIH HHS P01 AG003991NIA NIH HHS P01 AG026276NIA NIH HHS P50 AG005681
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the leading cause of dementia, accounting for 60-70% of all cases [Hebert et al., 2003, 1]. The need for effective therapies for AD is great. Current approaches, including cholinesterase inhibitors and N-methyl-d-aspartate (NMDA) receptor antagonists, are symptomatic treatments for AD but do not prevent disease progression. Many diagnostic and therapeutic approaches to AD are currently changing due to the knowledge that underlying pathology starts 10 to 20 years before clinical signs of dementia appear [Holtzman et al., 2011, 2]. New therapies which focus on prevention or delay of the onset or cognitive symptoms are needed. Recent advances in the identification of AD biomarkers now make it possible to detect AD pathology in the preclinical stage of the disease, in cognitively normal (CN) individuals; this biomarker data should be used in the selection of high-risk populations for clinical trials. In vivo visualization of AD neuropathology and biological, biochemical or physiological confirmation of the effects of treatment likely will substantially improve development of novel pharmaceuticals. Positron emission tomography (PET) is the leading neuroimaging tool to detect and provide quantitative measures of AD amyloid pathology in vivo at the early stages and follow its course longitudinally. This article is part of a Special Issue entitled: Imaging Brain Aging and Neurodegenerative disease.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBiomarkersBrainDisease ProgressionHumansPositron-Emission TomographyAmyloid beta-PeptidesBiomarkers

Identifiers

PMID22108203
PMCPMC3264790

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.