Greta Hultqvist

Senior Lecturer/ docent

Uppsala University

Sweden

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Greta Hultqvist is a Senior Lecturer and docent at Uppsala University in Sweden. Her research focuses on developing innovative therapies for Alzheimer's disease, including bispecific brain-penetrant antibodies, antibody radioligands for PET imaging, and novel therapeutic approaches to modulate amyloid beta and α-Synuclein interactions. Dr. Hultqvist's work aims to elucidate the underlying mechanisms of Alzheimer's pathology and enhance treatment efficacy through advanced antibody engineering.

Articles (17)

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2025

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2022

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2022

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2022

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2021

Collaborators (5)

Enrica Cerilli

Uppsala University

SWEDEN

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Jonas Eriksson

Uppsala University

SWEDEN

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Stina Syvänen

Associate Professor

Uppsala University

SWEDEN

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Dag Sehlin

Associate professor

Uppsala Universitet Medicinska fakulteten

SWEDEN

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Laura Suominen

University of Helsinki

FINLAND

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Greta Hultqvist

Research Interests

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About

Articles (17)

Bispecific brain-penetrant antibodies for treatment of Alzheimer’s disease

Somatostatin therapy, neprilysin activation, and amyloid beta reduction: A novel approach for Alzheimer's treatment

Serotransferrin enhances transferrin receptor-mediated brain uptake of antibodies

Altered amyloid-β structure markedly reduces gliosis in the brain of mice harboring the Uppsala APP deletion

A charged tail on anti-α-Synuclein antibodies does not enhance their affinity to α-Synuclein fibrils

Early Astrocytic Dysfunction Is Associated with Mistuned Synapses as well as Anxiety and Depressive-Like Behavior in the App<sup>NL-F</sup>Mouse Model of Alzheimer's Disease

A single‐chain fragment constant design enables easy production of a monovalent blood–brain barrier transporter and provides an improved brain uptake at elevated doses

Development of brain-penetrable antibody radioligands for <i>in vivo</i> PET imaging of amyloid-β and tau.

Long-term effects of immunotherapy with a brain penetrating Aβ antibody in a mouse model of Alzheimer's disease.

Standardized Preclinical In Vitro Blood–Brain Barrier Mouse Assay Validates Endocytosis-Dependent Antibody Transcytosis Using Transferrin-Receptor-Mediated Pathways

Multivalent design of the monoclonal SynO2 antibody improves binding strength to soluble α-Synuclein aggregates

Blood-brain barrier penetrating neprilysin degrades monomeric amyloid-beta in a mouse model of Alzheimer's disease.

Introducing or removing heparan sulfate binding sites does not alter brain uptake of the blood-brain barrier shuttle scFv8D3.

A Brain-Targeting Bispecific-Multivalent Antibody Clears Soluble Amyloid-Beta Aggregates in Alzheimer’s Disease Mice

Reduction of αSYN Pathology in a Mouse Model of PD Using a Brain-Penetrating Bispecific Antibody

In vivo imaging of alpha-synuclein with antibody-based PET.

Novel multivalent design of a monoclonal antibody improves binding strength to soluble aggregates of amyloid beta.

Collaborators (5)

Enrica Cerilli

Jonas Eriksson

Stina Syvänen

Dag Sehlin

Laura Suominen

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