Evidence map›Paper›PMID 22229116›Full record

ReviewCold Spring Harbor perspectives in medicine2011

Neuropathological alterations in Alzheimer disease.

Alberto Serrano-Pozo, Matthew P Frosch, Eliezer Masliah, Bradley T Hyman

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,760 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,760citing papers in PubMed, 2 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

1,760 citing papers in PubMed, 2 syntheses or guidelines pooled it, 3,323 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
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  6. Article
  7. Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  8. Review
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  11. Holdfast-Derived Lipid Extract from the Patagonian MacroalgaPharmaceuticals (Basel, Switzerland) · 2026
    Article
  12. Review
  13. Review
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1,700 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

4 authors at 3 institutions in 1 country.

Alberto Serrano-PozoAlzheimer Research Unit of the MassGeneral Institute for Neurodegenerative Disease, Department of Neurology of the Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA, 02129-4404.
Matthew P Frosch
Eliezer Masliah
Bradley T Hyman
MaineGeneral Medical Center · USMassachusetts General Hospital · USUniversity of California, San Diego · US

Funding

RECRUITMENT COREU19AG010483 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FELDMAN, HOWARD · 2013 to 2020
$80.6M
VIRUS-INDUCED BRAIN PATHOLOGYP50AG005131 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GALASKO, DOUGLAS R · 1985 to 2018
$55.4M
THE ROLE OF ADVANCED CAA IN ALZHEIMER'S DEMENTIAP50AG005134 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI GOMEZ-ISLA, TERESA · 1985 to 2018
$42.1M
Tissue Culture CoreP01AG022074 · NIA · J. DAVID GLADSTONE INSTITUTES · PI MUCKE, LENNART · 2003 to 2012
$27.0M
Viral VectorsP01AG010435 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TUSZYNSKI, MARK H. · 1991 to 2014
$20.9M
La Jolla Interdisciplinary Neuroscience Center Cores - Vital VP30NS057096 · NINDS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI LIPTON, STUART A · 2006 to 2010
$12.7M
NEUROPATHOLOGICAL ALTERATIONS IN ALZHEIMERS DISEASER01AG008487 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1995 to 2010
$5.4M
a-synuclein clearance strategies for the treatment of Lewy body disease.R37AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MASLIAH, ELIEZER · 2006 to 2014
$2.7M
PATHOLOGICAL ALTERATIONS IN ALZHEIMER'S DISEASER29AG008487 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T · 1989 to 1993
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NIA NIH HHS AG08487NIA NIH HHS AG10435NIA NIH HHS AG18840NIA NIH HHS AG22074NIA NIH HHS AG5131NIA NIH HHS P01 AG010435NIA NIH HHS P01 AG022074NIA NIH HHS P50 AG005131NIA NIH HHS P50 AG005134NIA NIH HHS P50AG05134NIA NIH HHS R01 AG008487NIA NIH HHS R37 AG018440NIA NIH HHS U19 AG010483NINDS NIH HHS NS057096NINDS NIH HHS P30 NS057096
6 · The paper itself

Abstract

The neuropathological hallmarks of Alzheimer disease (AD) include "positive" lesions such as amyloid plaques and cerebral amyloid angiopathy, neurofibrillary tangles, and glial responses, and "negative" lesions such as neuronal and synaptic loss. Despite their inherently cross-sectional nature, postmortem studies have enabled the staging of the progression of both amyloid and tangle pathologies, and, consequently, the development of diagnostic criteria that are now used worldwide. In addition, clinicopathological correlation studies have been crucial to generate hypotheses about the pathophysiology of the disease, by establishing that there is a continuum between "normal" aging and AD dementia, and that the amyloid plaque build-up occurs primarily before the onset of cognitive deficits, while neurofibrillary tangles, neuron loss, and particularly synaptic loss, parallel the progression of cognitive decline. Importantly, these cross-sectional neuropathological data have been largely validated by longitudinal in vivo studies using modern imaging biomarkers such as amyloid PET and volumetric MRI.

Indexed as

AgingAlzheimer DiseaseCerebral Amyloid AngiopathyCognitive DysfunctionHumansLewy Body DiseaseMagnetic Resonance ImagingNeurofibrillary TanglesPlaque, AmyloidPositron-Emission Tomography

Identifiers

PMID22229116
PMCPMC3234452
OpenAlexW2096963202

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.