Evidence map›Paper›PMID 31306129›Full record

ReviewJournal of Alzheimer's disease : JAD2019

Endothelial Mitochondrial Dysfunction in Cerebral Amyloid Angiopathy and Alzheimer's Disease.

Rebecca Parodi-Rullán, Je Yeong Sone, Silvia Fossati

Abstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
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  5. The evolving landscape of amyloid-targeting therapies in Alzheimer's disease: progress and challenges.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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13 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 at 1 institution in 1 country.

Rebecca Parodi-RullánAlzheimer's Center at Temple, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Je Yeong SoneDepartment of Psychiatry, Center for Brain Health, NYU School of Medicine, New York, NY, USA.
Silvia FossatiAlzheimer's Center at Temple, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Temple University · US

Funding

Potentiation of CAA-mediated endothelial dysfunction by cardiovascular risk factorsR01NS104127 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI FOSSATI, SILVIA · 2018 to 2022
$3.0M
Targeting carbonic anhydrases in Alzheimer's diseaseR01AG062572 · NIA · TEMPLE UNIV OF THE COMMONWEALTH · PI FOSSATI, SILVIA · 2019 to 2023
$2.3M
NIA NIH HHS R01 AG062572NINDS NIH HHS R01 NS104127
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most prevalent form of dementia. Cerebrovascular dysfunction is one of the earliest events in the pathogenesis of AD, as well as in vascular and mixed dementias. Cerebral amyloid angiopathy (CAA), the deposition of amyloid around cerebral vessels, is observed in up to 90% of AD patients and in approximately 50% of elderly individuals over 80 years of age. CAA is a strong contributor to vascular dysfunction in AD. CAA-laden brain vessels are characterized by dysfunctional hemodynamics and leaky blood-brain barrier (BBB), contributing to clearance failure and further accumulation of amyloid-β (Aβ) in the cerebrovasculature and brain parenchyma. Mitochondrial dysfunction is increasingly recognized as an important early initiator of the pathogenesis of AD and CAA. The objective of this review is to discuss the effects of Aβ on cerebral microvascular cell function, focusing on its impact on endothelial mitochondria. After introducing CAA and its etiology and genetic risk factors, we describe the pathological relationship between cerebrovascular amyloidosis and brain microvascular endothelial cell dysfunction, critically analyzing its roles in disease progression, hypoperfusion, and BBB integrity. Then, we focus on discussing the effect of Aβ challenge on endothelial mitochondrial dysfunction pathways, and their contribution to the progression of neurovascular dysfunction in AD and dementia. Finally, we report potential pharmacological and non-pharmacological mitochondria-targeted therapeutic strategies which may help prevent or delay cerebrovascular failure.

Indexed as

Alzheimer DiseaseAnimalsApoptosisBlood-Brain BarrierBrainCerebral Amyloid AngiopathyEndothelial CellsHumansMitochondriaReactive Oxygen SpeciesReactive Oxygen SpeciesAlzheimer’s diseaseamyloidapoptosisblood-brain barriercerebral amyloid angiopathyendothelial cellsmitochondrianeurodegenerationreactive nitrogen speciesreactive oxygen species

Identifiers

PMID31306129
PMCPMC6917858
OpenAlexW2959473339

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.