Evidence map›Paper›PMID 36529160›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2023

Vascular contributions to Alzheimer's disease.

Laura B Eisenmenger, Anthony Peret, Bolanle M Famakin, Alma Spahic, Grant S Roberts, Jeremy H Bockholt, Kevin M Johnson, Jane S Paulsen

Open access · greenAbstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 2 pooled it
14.9field-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

101 citing papers in PubMed, 2 syntheses or guidelines pooled it, 143 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Sleep apnea in REM sleep as an amplifier of vascular contributions to Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Neurovascular decoupling: An early indicator of cognitive decline.Journal of Alzheimer's disease : JAD · 2026
    Article
  17. Review
  18. Article
  19. Article
  20. Review

41 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

8 authors at 2 institutions in 1 country.

Laura B EisenmengerDepartment of Radiology, University of Wisconsin-Madison, Madison, Wisconsin.
Anthony PeretDepartment of Radiology, University of Wisconsin-Madison, Madison, Wisconsin.
Bolanle M FamakinDepartment of Neurology, University of Wisconsin-Madison, Madison, Wisconsin.
Alma SpahicDepartment of Medical Physics, University of Wisconsin-Madison, Madison, Wisconsin.
Grant S RobertsDepartment of Medical Physics, University of Wisconsin-Madison, Madison, Wisconsin.
Jeremy H BockholtTri-Institutional Center for Translational Research in Neuroimaging and Data Science (TReNDS), Georgia State University, Georgia Institute of Technology, and Emory University, Atlanta, Georgia.
Kevin M JohnsonDepartment of Medical Physics, University of Wisconsin-Madison, Madison, Wisconsin.
Jane S PaulsenDepartment of Neurology, University of Wisconsin-Madison, Madison, Wisconsin. Electronic address: paulsen@neurology.wisc.edu.
University of Wisconsin–Madison · USEmory University · US

Funding

University of Wisconsin Institute for Clinical and Translational ResearchUL1TR002373 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI ELIZABETH S BURNSIDE, Allan R. Brasier · 2017 to 2026
$75.9M
Wisconsin Alzheimer's Disease Research CenterP30AG062715 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI Barbara Brigitta Bendlin · 2019 to 2026
$34.5M
Unraveling the earliest phases of vascular cognitive impairment and dementia using CADASIL--a monogenic form of small vessel cerebrovascular diseaseRF1AG074608 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI GESCHWIND, MICHAEL D, PAULSEN, JANE S · 2021 to 2025
$21.2M
Institutional Career Development CoreKL2TR002374 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI Bo Liu, Marin Leigh Schweizer · 2017 to 2026
$9.7M
Non-Invasive Imaging Markers to Elicit the Role of Vascular Involvement in Alzheimer’s DiseaseR01AG075788 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI Kevin Michael Johnson · 2022 to 2026
$3.2M
Preparing for preventive clinical trials in Huntington's diseaseU01NS105509 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI PAULSEN, JANE S · 2020 to 2025
$2.5M
Statistical disease modeling and clinimetrics to prepare for preventive trials in huntington diseaseU01NS103475 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI PAULSEN, JANE S · 2020 to 2022
$1.7M
Multi-Parametric Imaging of Systemic Cardiovascular and Cerebrovascular Health in Alzheimer's DiseaseF31AG071183 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI ROBERTS, GRANT S. · 2021 to 2022
$70k
NCATS NIH HHS KL2 TR002374NCATS NIH HHS UL1 TR002373NIA NIH HHS F31 AG071183NIA NIH HHS P30 AG062715NIA NIH HHS R01 AG075788NIA NIH HHS RF1 AG074608NINDS NIH HHS U01 NS103475NINDS NIH HHS U01 NS105509
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common cause of dementia and is characterized by progressive neurodegeneration and cognitive decline. Understanding the pathophysiology underlying AD is paramount for the management of individuals at risk of and suffering from AD. The vascular hypothesis stipulates a relationship between cardiovascular disease and AD-related changes although the nature of this relationship remains unknown. In this review, we discuss several potential pathological pathways of vascular involvement in AD that have been described including dysregulation of neurovascular coupling, disruption of the blood brain barrier, and reduced clearance of metabolite waste such as beta-amyloid, a toxic peptide considered the hallmark of AD. We will also discuss the two-hit hypothesis which proposes a 2-step positive feedback loop in which microvascular insults precede the accumulation of Aß and are thought to be at the origin of the disease development. At neuroimaging, signs of vascular dysfunction such as chronic cerebral hypoperfusion have been demonstrated, appearing early in AD, even before cognitive decline and alteration of traditional biomarkers. Cerebral small vessel disease such as cerebral amyloid angiopathy, characterized by the aggregation of Aß in the vessel wall, is highly prevalent in vascular dementia and AD patients. Current data is unclear whether cardiovascular disease causes, precipitates, amplifies, precedes, or simply coincides with AD. Targeted imaging tools to quantitatively evaluate the intracranial vasculature and longitudinal studies in individuals at risk for or in the early stages of the AD continuum could be critical in disentangling this complex relationship between vascular disease and AD.

Indexed as

Alzheimer DiseaseCardiovascular DiseasesCognitive DysfunctionBlood-Brain BarrierBrainHumans

Identifiers

PMID36529160
PMCPMC10481451
OpenAlexW4311549226

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.