Evidence map›Paper›PMID 31379558›Full record

ArticleFrontiers in aging neuroscience2019

Liver Dysfunction as a Novel Player in Alzheimer's Progression: Looking Outside the Brain.

Lisbell D Estrada, Pablo Ahumada, Daniel Cabrera, Juan P Arab

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 2 pooled it
8.7field-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

93 citing papers in PubMed, 2 syntheses or guidelines pooled it, 150 citations in OpenAlex.

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  11. Mechanistic insights into the liver-brain axis during chronic liver disease.Nature reviews. Gastroenterology & hepatology · 2026
    Review
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33 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

4 authors at 2 institutions in 1 country.

Lisbell D EstradaBionanotechnology Laboratory, Integrative Center for Applied Biology and Chemistry (CIBQA), Department of Chemical & Biological Sciences, Universidad Bernardo O'Higgins, Santiago, Chile.
Pablo AhumadaBionanotechnology Laboratory, Integrative Center for Applied Biology and Chemistry (CIBQA), Department of Chemical & Biological Sciences, Universidad Bernardo O'Higgins, Santiago, Chile.
Daniel CabreraBionanotechnology Laboratory, Integrative Center for Applied Biology and Chemistry (CIBQA), Department of Chemical & Biological Sciences, Universidad Bernardo O'Higgins, Santiago, Chile.
Juan P ArabLaboratório de Hepatologia Experimental, Gastroenterology Department, Facultad de Medicina, Centro de Envejecimiento y Regeneración (CARE Chile-UC), P. Universidad Catolica de Chile, Santiago, Chile.
Universidad Bernardo O'Higgins · CLPontificia Universidad Católica de Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) afflicts an estimated 20 million people worldwide and is the fourth-leading cause of death in the developed world. The most common cause of dementia in older individuals, AD is characterized by neuropathologies including synaptic and neuronal degeneration, amyloid plaques, and neurofibrillary tangles (NTFs). Amyloid plaques are primarily composed of amyloid-beta peptide (Aβ), which accumulates in the brains of patients with AD. Further, small aggregates termed Aβ oligomers are implicated in the synaptic loss and neuronal degeneration underlying early cognitive impairments. Whether Aβ accumulates in part because of dysregulated clearance from the brain remains unclear. The flow of substances (e.g., nutrients, drugs, toxins) in and out of the brain is mediated by the blood-brain-barrier (BBB). The BBB exhibits impairment in AD patients and animal models. The effect of BBB impairment on Aβ, and whether BBB function is affected by non-neurological pathologies that impair peripheral clearance requires further investigation. In particular, impaired peripheral clearance is a feature of nonalcoholic fatty liver disease (NAFLD), a spectrum of liver disorders characterized by accumulation of fat in the liver accompanied by varying degrees of inflammation and hepatocyte injury. NAFLD has reached epidemic proportions, with an estimated prevalence between 20% and 30% of the general population. This chronic condition may influence AD pathogenesis. This review article summarizes the current state of the literature linking NAFLD and AD, highlighting the role of the major Aβ efflux and clearance protein, the LRP-1 receptor, which is abundantly expressed in liver, brain, and vasculature.

Indexed as

Alzheimer’samyloid betaBBBLRP-1NAFLD

Identifiers

PMID31379558
PMCPMC6650779
OpenAlexW2959600071

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.