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The Neuroprotective Effect of Neural Cell Adhesion Molecule L1 in the Hippocampus of Aged Alzheimer's Disease Model Mice.
Aksic, Miljana; Jakovcevski, Igor; Hamad, Mohammad I K; Jakovljevic, Vladimir; Stankovic, Sanja; Vulovic, Maja.
Afiliación
  • Aksic M; Center for Medical Biochemistry, University Clinical Center of Serbia, 11000 Belgrade, Serbia.
  • Jakovcevski I; Institut für Anatomie und Klinische Morphologie, Universität Witten/Herdecke, 58455 Witten, Germany.
  • Hamad MIK; Department of Neuroanatomy and Molecular Brain Research, Institute of Anatomy, Ruhr Universität Bochum, 44801 Bochum, Germany.
  • Jakovljevic V; Department of Anatomy, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain P.O. Box 64141, United Arab Emirates.
  • Stankovic S; Center of Excellence for Redox Balance Research, Cardiovascular and Metabolic Disorders, Department of Physiology, Faculty of Medical Sciences, University of Kragujevac, 34000 Kragujevac, Serbia.
  • Vulovic M; Center for Medical Biochemistry, University Clinical Center of Serbia, 11000 Belgrade, Serbia.
Biomedicines ; 12(8)2024 Aug 01.
Article en En | MEDLINE | ID: mdl-39200191
ABSTRACT
Alzheimer's disease (AD) is a severe neurodegenerative disorder and the most common form of dementia, causing the loss of cognitive function. Our previous study has shown, using a doubly mutated mouse model of AD (APP/PS1), that the neural adhesion molecule L1 directly binds amyloid peptides and decreases plaque load and gliosis when injected as an adeno-associated virus construct (AAV-L1) into APP/PS1 mice. In this study, we microinjected AAV-L1, using a Hamilton syringe, directly into the 3-month-old APP/PS1 mouse hippocampus and waited for a year until significant neurodegeneration developed. We stereologically counted the principal neurons and parvalbumin-positive interneurons in the hippocampus, estimated the density of inhibitory synapses around principal cells, and compared the AAV-L1 injection models with control injections of green fluorescent protein (AAV-GFP) and the wild-type hippocampus. Our results show that there is a significant loss of granule cells in the dentate gyrus of the APP/PS1 mice, which was improved by AAV-L1 injection, compared with the AAV-GFP controls (p < 0.05). There is also a generalized loss of parvalbumin-positive interneurons in the hippocampus of APP/PS1 mice, which is ameliorated by AAV-L1 injection, compared with the AAV-GFP controls (p < 0.05). Additionally, AAV-L1 injection promotes the survival of inhibitory synapses around the principal cells compared with AAV-GFP controls in all three hippocampal subfields (p < 0.01). Our results indicate that L1 promotes neuronal survival and protects the synapses in an AD mouse model, which could have therapeutic implications.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Biomedicines Año: 2024 Tipo del documento: Article Pais de publicación: Suiza

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Biomedicines Año: 2024 Tipo del documento: Article Pais de publicación: Suiza