Evidence map›Paper›PMID 35248124›Full record

ReviewMolecular neurodegeneration2022

Alzheimer's disease - the journey of a healthy brain into organ failure.

Todd E Golde

Open access · goldAbstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 1% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
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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

1 author at 1 institution in 1 country.

Todd E GoldeDepartments of Neuroscience and Neurology, Evelyn F. and William L. McKnight Brain Institute, Norman Fixel Institute for Neurological Diseases, Center for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, Fl, USA. tgolde@ufl.edu.
University of Florida · US

Funding

Social Determinants of Health, Race/Ethnicity, and White Matter HyperintensitiesP30AG066506 · NIA · UNIVERSITY OF FLORIDA · PI Rosie E Curiel Cid · 2020 to 2026
$25.6M
Integrating the exposome and methylome to inform brain molecular changes in ADRD across established diverse cohorts.U01AG046139 · NIA · UNIVERSITY OF FLORIDA · PI ERTEKIN-TANER, NILUFER, FUNK, CORY · 2013 to 2022
$24.6M
Immunotherapy targeting the HPA axis in Alzheimer’s diseaseRF1AG064942 · NIA · UNIVERSITY OF FLORIDA · PI BIZON, JENNIFER LYNN, GOLDE, TODD E · 2019 to 2019
$4.0M
Modulation of Alzheimers disease by Herpes simplex virus infection R01AG062514 · NIA · UNIVERSITY OF WASHINGTON · PI DARVAS, MARTIN C, FUNK, CORY · 2019 to 2023
$2.7M
APOE as a modifier of prion-like spread in dementiaRF1AG057933 · NIA · UNIVERSITY OF FLORIDA · PI BORCHELT, DAVID R, CHAKRABARTY, PARAMITA · 2018 to 2018
$2.6M
Elucidating factors that modulate tauopathy and cellular degeneration to guide therapeutic developmentRF1AG064914 · NIA · UNIVERSITY OF FLORIDA · PI GOLDE, TODD E, LEWIS, JADA M · 2019 to 2019
$2.5M
NIA NIH HHS P30 AG066506NIA NIH HHS P30AG066506NIA NIH HHS R01 AG062514NIA NIH HHS RF1 AG057933NIA NIH HHS RF1AG057933NIA NIH HHS RF1 AG064914NIA NIH HHS RF1AG064914NIA NIH HHS RF1 AG064942NIA NIH HHS RF1AG064942NIA NIH HHS U01 AG046139NIA NIH HHS U01AG046139
6 · The paper itself

Abstract

As the most common dementia, Alzheimer's disease (AD) exacts an immense personal, societal, and economic toll. AD was first described at the neuropathological level in the early 1900s. Today, we have mechanistic insight into select aspects of AD pathogenesis and have the ability to clinically detect and diagnose AD and underlying AD pathologies in living patients. These insights demonstrate that AD is a complex, insidious, degenerative proteinopathy triggered by Aβ aggregate formation. Over time Aβ pathology drives neurofibrillary tangle (NFT) pathology, dysfunction of virtually all cell types in the brain, and ultimately, overt neurodegeneration. Yet, large gaps in our knowledge of AD pathophysiology and huge unmet medical need remain. Though we largely conceptualize AD as a disease of aging, heritable and non-heritable factors impact brain physiology, either continuously or at specific time points during the lifespan, and thereby alter risk for devolvement of AD. Herein, I describe the lifelong journey of a healthy brain from birth to death with AD, while acknowledging the many knowledge gaps that remain regarding our understanding of AD pathogenesis. To ensure the current lexicon surrounding AD changes from inevitable, incurable, and poorly manageable to a lexicon of preventable, curable, and manageable we must address these knowledge gaps, develop therapies that have a bigger impact on clinical symptoms or progression of disease and use these interventions at the appropriate stage of disease.

Indexed as

Alzheimer DiseaseAgingAmyloid beta-PeptidesBrainHumansNeurofibrillary Tanglestau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer’s DiseaseAmyloidNeurodegenerationOrgan failureProteinopathyRisk factorsTau

Identifiers

PMID35248124
PMCPMC8898417
OpenAlexW4220985829

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.