Taliglucerase Alfa Reduces Amyloid-β Burden by Restoring Autophagic Pathways in a Neuronal Model of Alzheimer's Disease.

Çağrı Özkurt, Selma Köse, Çimen Karasu, Arjan Kortholt, Pelin Kelicen-Uğur

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Article in Neurochemical research, 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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0citing papers in PubMed

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5 · Who and what money

Authors and funding

5 authors.

Çağrı ÖzkurtDepartment of Pharmacology, Faculty of Pharmacy, Hacettepe University, Ankara, Turkey.ORCID http://orcid.org/0000-0001-9641-6745

Selma KöseDepartment of Pharmacology, Faculty of Pharmacy, Lokman Hekim University, Ankara, Turkey.ORCID http://orcid.org/0000-0001-6682-3569

Çimen KarasuDepartment of Medical Pharmacology, Faculty of Medicine, Gazi University, Ankara, Turkey.ORCID http://orcid.org/0000-0002-0954-8465

Arjan KortholtYETEM-Innovative Technologies Application and Research Centre, Suleyman Demirel University, Isparta, Turkey.ORCID http://orcid.org/0000-0001-8174-6397

Pelin Kelicen-UğurDepartment of Pharmacology, Faculty of Pharmacy, Hacettepe University, Ankara, Turkey. pkelicen@hacettepe.edu.tr.ORCID http://orcid.org/0000-0003-1661-0631

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intraneuronal amyloid-beta (Aβ) accumulation and autophagic dysfunction are key pathological features of Alzheimer's disease (AD). Mutations in GBA1, which encodes the lysosomal enzyme β-glucocerebrosidase (GCase), are linked to several neurodegenerative disorders, but the role of GCase in AD remains incompletely understood. In this exploratory, proof-of-concept study, we investigated whether taliglucerase alfa (TAL), a recombinant human GCase, may influence intracellular Aβ accumulation by modulating autophagy pathways in a neuronal AD model. Endogenous Aβ accumulation was induced in mouse hippocampal neuronal cells (HT-22) by exposure to low-molecular-weight Aβ

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesGlucosylceramidaseHippocampusPeptide FragmentsAutophagyCell LineNeuronsRecombinant ProteinsAmyloid beta-PeptidesGlucosylceramidasePeptide FragmentsRecombinant ProteinsAlzheimer’s diseaseAutophagyEnzyme replacement therapyLysosomal storage disorderTaliglucerase alfaβ-Glucocerebrosidase

Identifiers

PMID42223785

DOI10.1007/s11064-026-04792-w

PMCPMC13226380

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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.