Evidence map›Paper›PMID 39769398›Full record

ReviewInternational journal of molecular sciences2024

The Emerging Role of PCSK9 in the Pathogenesis of Alzheimer's Disease: A Possible Target for the Disease Treatment.

Gabriella Testa, Serena Giannelli, Erica Staurenghi, Rebecca Cecci, Lucrezia Floro, Paola Gamba, Barbara Sottero, Gabriella Leonarduzzi

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–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

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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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.

Gabriella TestaDepartment of Clinical and Biological Sciences, University of Turin, San Luigi Hospital, 10043 Orbassano, Italy.ORCID 0000-0002-2835-2804
Serena GiannelliDepartment of Clinical and Biological Sciences, University of Turin, San Luigi Hospital, 10043 Orbassano, Italy.ORCID 0000-0002-8364-9301
Erica StaurenghiDepartment of Clinical and Biological Sciences, University of Turin, San Luigi Hospital, 10043 Orbassano, Italy.ORCID 0000-0001-5035-7401
Rebecca CecciDepartment of Clinical and Biological Sciences, University of Turin, San Luigi Hospital, 10043 Orbassano, Italy.ORCID 0009-0008-7869-9946
Lucrezia FloroDepartment of Clinical and Biological Sciences, University of Turin, San Luigi Hospital, 10043 Orbassano, Italy.ORCID 0009-0000-3684-0923
Paola GambaDepartment of Clinical and Biological Sciences, University of Turin, San Luigi Hospital, 10043 Orbassano, Italy.ORCID 0000-0003-2715-5435
Barbara SotteroDepartment of Clinical and Biological Sciences, University of Turin, San Luigi Hospital, 10043 Orbassano, Italy.ORCID 0000-0003-3323-3110
Gabriella LeonarduzziDepartment of Clinical and Biological Sciences, University of Turin, San Luigi Hospital, 10043 Orbassano, Italy.ORCID 0000-0002-3422-821X

Funding

University of Turin LEOG_RILO_23_01; GAMP_RILO_23_01; SOTB_RILO_23_01; LEOG_RF_CLINIC_23_01
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a multifactorial neurodegenerative disease mainly caused by β-amyloid (Aβ) accumulation in the brain. Among the several factors that may concur to AD development, elevated cholesterol levels and brain cholesterol dyshomeostasis have been recognized to play a relevant role. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a protein primarily known to regulate plasma low-density lipoproteins (LDLs) rich in cholesterol and to be one of the main causes of familial hypercholesterolemia. In addition to that, PCSK9 is also recognized to carry out diverse important activities in the brain, including control of neuronal differentiation, apoptosis, and, importantly, LDL receptors functionality. Moreover, PCSK9 appeared to be directly involved in some of the principal processes responsible for AD development, such as inflammation, oxidative stress, and Aβ deposition. On these bases, PCSK9 management might represent a promising approach for AD treatment. The purpose of this review is to elucidate the role of PCSK9, whether or not cholesterol-related, in AD pathogenesis and to give an updated overview of the most innovative therapeutic strategies developed so far to counteract the pleiotropic activities of both humoral and brain PCSK9, focusing in particular on their potentiality for AD management.

Indexed as

Alzheimer DiseaseProprotein Convertase 9Amyloid beta-PeptidesAnimalsBrainCholesterolHumansPCSK9 InhibitorsAmyloid beta-PeptidesCholesterolPCSK9 InhibitorsPCSK9 protein, humanProprotein Convertase 9Alzheimer’s diseaseApoEcholesterolLDL receptorsneuroinflammationoxidative stressPCSK9PCSK9 targeting therapiesβ-amyloid

Identifiers

PMID39769398
PMCPMC11727734

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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 OpenQuestion graph.