Evidence mapPaperPMID 41711028Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2026

Renin-Angiotensin-Aldosterone System in Preeclampsia: Pathophysiological Insights and Links to Vascular Dementia.

Jenny Lutshumba, Elizabeth Mirsky, Kelsey A Bullens, Emma G Smith, Esther L Ndashaala, Robin Finch

Abstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Jenny LutshumbaDepartment of Neurology (J.L., E.G.S.), University of Kentucky, Lexington.ORCID 0000-0002-6874-5565
Elizabeth MirskyDepartment of Obstetrics and Gynecology (E.M.), University of Kentucky, Lexington.ORCID 0000-0001-8746-8471
Kelsey A BullensDepartment of Physiology (J.L., K.A.B.), University of Kentucky, Lexington.ORCID 0000-0003-1438-874X
Emma G SmithDepartment of Neurology (J.L., E.G.S.), University of Kentucky, Lexington.
Esther L NdashaalaDepartment of Dietetics and Human Nutrition (E.L.N.), University of Kentucky, Lexington.
Robin FinchDepartment of Pediatrics (R.F.), University of Kentucky, Lexington., University of Kentucky, Lexington.ORCID 0000-0002-9972-7677

Funding

Biomarkers to Track Effective Interventions that Delay Dementia Onset in Participants of the "Risk Reduction for Alzheimer's Disease (rrAD)" TrialRF1AG084134 · NIA · UNIVERSITY OF KENTUCKY · PI DWIGHT C. German, Ann Marie Stowe · 2023 to 2023
$2.3M
NIA NIH HHS L30 AG089724NIA NIH HHS RF1 AG084134
6 · The paper itself

Abstract

Preeclampsia, a condition characterized by new-onset hypertension during pregnancy and ≥1 indices of organ damage, is a major driver of both short- and long-term maternal health outcomes. Individuals with a history of preeclampsia are at increased risk for cardiovascular, renal, and other chronic diseases. Recent studies have linked preeclampsia history with increased risk of dementia later in life, underscoring the importance of new guidelines emphasizing blood pressure control to reduce the risk of cognitive decline. Unfortunately, neither the mechanisms underlying the causes of preeclampsia nor their links with cognitive function are well understood. Vascular contributions to cognitive impairment and dementia are a type of dementia caused by reduced cerebral blood flow, often resulting from vascular dysfunction associated with small vessel damage or chronic hypertension. The renin-angiotensin-aldosterone system (RAAS) is a hormone system with a major role in regulating blood pressure, fluid homeostasis, and vascular function inside and outside of pregnancy. The RAAS is markedly activated during pregnancy; preeclampsia is associated with disruptions in the normal activity of the RAAS, including excessive Ang (angiotensin) II type 1 receptor signaling, and loss of protective effects of Ang-(1-7) and Ang II type 2 receptors. Preexisting hypertension may impair the normal RAAS response to pregnancy, increasing susceptibility to vascular damage both during and after pregnancy. Results from human and animal studies indicate that dysregulation of the RAAS is a shared pathway underlying vascular dysfunction in both preeclampsia and vascular contributions to cognitive impairment and dementia, suggesting a mechanistic link between these 2 conditions. Persistent endothelial damage, impaired vascular remodeling, and chronic activation of Ang II type 1 and mineralocorticoid receptor signaling may increase long-term risk. This connection underscores the importance of monitoring and managing blood pressure during pregnancy and in women with a history of preeclampsia to mitigate the risk of dementia.

Indexed as

Blood PressureCognitionDementia, VascularPre-EclampsiaRenin-Angiotensin SystemAnimalsFemaleHumansPregnancyRisk FactorsSignal Transductionagingangiotensinscerebral small vessel diseasecognitive dysfunctionendotheliumhypertensionpregnancy

Identifiers

PMID41711028
PMCPMC13195582

What Socratic holds

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Registered trials

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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 Socratic graph.