Per Nilsson

Team leader, Assoc Prof

Karolinska Institutet

Sweden

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About

Per Nilsson is an Associate Professor and Team Leader at Karolinska Institutet in Sweden. His research focuses on the dopaminergic system, amyloid-β dynamics, and the pathophysiological mechanisms underlying Alzheimer's disease. Recent publications explore the roles of autophagy, intracellular transport of APP, and mitochondrial functions in Alzheimer’s pathology.

Articles (15)

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2024

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2024

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2024

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2024

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2024

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2023

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2023

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2023

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2023

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2023

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2022

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2022

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2021

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2020

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2020

Collaborators (21)

Hugo Balleza-Tapia

Karolinska Institutet

SWEDEN

Per Nilsson

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Articles (15)

Signal peptide peptidase-like 2b modulates the amyloidogenic pathway and exhibits an Aβ-dependent expression in Alzheimer's disease

Inhibition of Autophagy Alters Intracellular Transport of APP Resulting in Increased APP Processing

The dopaminergic system promotes neprilysin-mediated degradation of amyloid-β in the brain

Divergent Age-Dependent Conformational Rearrangement within Aβ Amyloid Deposits in APP23, APPPS1, and AppNL-F Mice

DEAD Box Helicase 24 Is Increased in the Brain in Alzheimer’s Disease and AppN-LF Mice and Influences Presymptomatic Pathology

The Expression of the Endocannabinoid Receptors CB2 and GPR55 is Highly Increased during the Progression of Alzheimer’s Disease in AppNL-G-F Knock-In Mice

Molecular anatomy of adult mouse leptomeninges

Mitochondrial hypermetabolism precedes impaired autophagy and synaptic disorganization in App knock-in Alzheimer mouse models

Low dose of levetiracetam counteracts amyloid β-induced alterations of hippocampal gamma oscillations by restoring fast-spiking interneuron activity.

Feasibility and therapeutical potential of local intracerebral encapsulated cell biodelivery of BDNF to App<sup>NL-G-F</sup> knock-in Alzheimer mice.

Intranasal delivery of pro-resolving lipid mediators rescues memory and gamma oscillation impairment in AppNL-G-F/NL-G-F mice

Somatostatin-evoked Aβ catabolism in the brain: Mechanistic involvement of α-endosulfine-KATP channel pathway

Impaired spike-gamma coupling of area CA3 fast-spiking interneurons as the earliest functional impairment in the App<sup>NL-G-F</sup> mouse model of Alzheimer's disease.

Augmentation of Bri2 molecular chaperone activity against amyloid-β reduces neurotoxicity in mouse hippocampus in vitro

Amyloid Β-Peptide Increases Mitochondria-Endoplasmic Reticulum Contact Altering Mitochondrial Function and Autophagosome Formation in Alzheimer's Disease-Related Models

Collaborators (21)

Hugo Balleza-Tapia

Taija Makinen

Katrine Dahl Bjørnholm

Gefei Chen

Per Hammarstrom

Maria Ankarcrona

Maho Hamasaki

Francesca Del Gaudio

Simone Tambaro

Henrik Biverstal

Luis Enrique Arroyo-Garcia

Bernadette Schreiner

Luana Naia

Maarja Andaloussi Mäe

Eric Thelin

Makoto Shimozawa

Silvia Maioli

Axel Leppert

Bernd Schröder

Raúl Loera-Valencia

Takashi Saito

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