Evidence map›Paper›PMID 33444096›Full record

ReviewJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2021

Causes and consequences of baseline cerebral blood flow reductions in Alzheimer's disease.

Oliver Bracko, Jean C Cruz Hernández, Laibaik Park, Nozomi Nishimura, Chris B Schaffer

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
8.9field-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

82 citing papers in PubMed, 116 citations in OpenAlex.

  1. Trial
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  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
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  8. Article
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  16. Cortical OProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  17. Review
  18. Article
  19. Article
  20. Article

22 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

5 authors at 2 institutions in 1 country.

Oliver BrackoMeinig School of Biomedical Engineering, Cornell University, Ithaca, NY, USA.
Jean C Cruz HernándezCenter for Systems Biology and Wellman Center for Photomedicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Laibaik ParkFeil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY, USA.
Nozomi NishimuraMeinig School of Biomedical Engineering, Cornell University, Ithaca, NY, USA.ORCID 0000-0003-4342-9416
Chris B SchafferMeinig School of Biomedical Engineering, Cornell University, Ithaca, NY, USA.
Cornell University · USHarvard University · US

Funding

tPA and Cerebrovascular Regulation in a Model of β-amyloid PathologyR01NS097805 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI Laibaik Park · 2018 to 2026
$3.8M
STALLED CAPILLARY FLOW: A NOVEL MECHANISM FOR HYPOPERFUSION IN ALZHEIMER DISEASER01AG049952 · NIA · CORNELL UNIVERSITY · PI NISHIMURA, NOZOMI, SCHAFFER, CHRIS B · 2015 to 2025
$3.5M
The impact of microvascular (dys)regulation on cerebral flow and oxygen heterogeneityR01NS108472 · NINDS · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI BOAS, DAVID A, SCHAFFER, CHRIS B · 2018 to 2022
$3.2M
Supplement: Stalled capillary flow affects protein clearance by modulating interstitial fluid flowRF1AG049952 · NIA · CORNELL UNIVERSITY · PI NISHIMURA, NOZOMI, SCHAFFER, CHRIS B · 2021 to 2022
$2.6M
NIA NIH HHS R01 AG049952NIA NIH HHS RF1 AG049952NINDS NIH HHS R01 NS097805NINDS NIH HHS R01 NS108472
6 · The paper itself

Abstract

Reductions of baseline cerebral blood flow (CBF) of ∼10-20% are a common symptom of Alzheimer's disease (AD) that appear early in disease progression and correlate with the severity of cognitive impairment. These CBF deficits are replicated in mouse models of AD and recent work shows that increasing baseline CBF can rapidly improve the performance of AD mice on short term memory tasks. Despite the potential role these data suggest for CBF reductions in causing cognitive symptoms and contributing to brain pathology in AD, there remains a poor understanding of the molecular and cellular mechanisms causing them. This review compiles data on CBF reductions and on the correlation of AD-related CBF deficits with disease comorbidities (e.g. cardiovascular and genetic risk factors) and outcomes (e.g. cognitive performance and brain pathology) from studies in both patients and mouse models, and discusses several potential mechanisms proposed to contribute to CBF reductions, based primarily on work in AD mouse models. Future research aimed at improving our understanding of the importance of and interplay between different mechanisms for CBF reduction, as well as at determining the role these mechanisms play in AD patients could guide the development of future therapies that target CBF reductions in AD.

Indexed as

Cerebrovascular CirculationAlzheimer DiseaseAnimalsCerebrovascular DisordersDisease Models, AnimalHumansAlzheimer’s diseasecerebral blood flowcognitive impairmentin vivo 2-photon imagingmagnetic resonance imaging

Identifiers

PMID33444096
PMCPMC8221770
OpenAlexW3118792407

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.