<abstract xmlns="http://www.w3.org/1999/xhtml">

<p>Alzheimer’s disease (AD) is a devastating neurodegenerative disorder and the most common cause of elderly dementia. One of the main features of AD diseased brain are amyloid plaques, pathological depositions made of β-amyloid peptide, derived from β- amyloid precursor protein (APP). To assess how AD pathology affects synapses in the hippocampus, brain region to be one of the earliest with obvious pathological changes, we examined APPPS1 mice, transgeneticaly expressing human APP mutation (“Swedish mutation”) and human presenilin-1 mutation under the neuron-specific promoter, which develop AD symptoms early in life. We analyzed inhibitory and excitatory synapses using immunoflourescent staining and laser scanning confocal microscopy. In APPPS1 mice, inhibitory synaptic terminals labeled with vesicular inhibitory transmitter transporter (VGAT) were reduced in CA1 and CA3 regions of the hippocampus in APPPS1 mice compared to controls. This was true for both parvalbumin-positive and parvalbumin-negative terminals. On the other hand, excitatory synapses, coming from either hippocampal or entorhinal projections were similar between the genotypes. We conclude that first changes in the hippocampus caused by amyloid pathology affect inhibitory, but not excitatory synapses.</p>
</abstract>

Alzheimer’s disease (AD) is a devastating neurodegenerative disorder and the most common cause of elderly dementia. One of the main features of AD diseased brain are amyloid plaques, pathological depositions made of β-amyloid peptide, derived from β- amyloid precursor protein (APP). To assess how AD pathology affects synapses in the hippocampus, brain region to be one of the earliest with obvious pathological changes, we examined APPPS1 mice, transgeneticaly expressing human APP mutation (“Swedish mutation”) and human presenilin-1 mutation under the neuron-specific promoter, which develop AD symptoms early in life. We analyzed inhibitory and excitatory synapses using immunoflourescent staining and laser scanning confocal microscopy. In APPPS1 mice, inhibitory synaptic terminals labeled with vesicular inhibitory transmitter transporter (VGAT) were reduced in CA1 and CA3 regions of the hippocampus in APPPS1 mice compared to controls. This was true for both parvalbumin-positive and parvalbumin-negative terminals. On the other hand, excitatory synapses, coming from either hippocampal or entorhinal projections were similar between the genotypes. We conclude that first changes in the hippocampus caused by amyloid pathology affect inhibitory, but not excitatory synapses.

Inhibitory, But Not Excitatory Synapses Are Reduced in the Hippocampus of the Six-Month-Old Alzheimer’s Disease Model Mouse

Faculty of Medical Sciences, Department of Anatomy

Experimental and Applied Biomedical Research (EABR)

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Alzheimer’s disease (AD) is a devastating neurodegenerative disorder and the most common cause of elderly dementia. One of the main features of AD diseased...

Inhibitory, But Not Excitatory Synapses Are Reduced in the Hippocampus of the Six-Month-Old Alzheimer’s Disease Model Mouse

Pubblicato online: 01 mag 2023

Pagine: -

Ricevuto: 06 mar 2023

Accettato: 05 apr 2023

DOI: https://doi.org/10.2478/sjecr-2023-0003

Parole chiave
Alzheimer’s disease, hippocampus, GABAergic interneurons, synapses, vesicular transmitter transporters

© 2023 Miljana Aksic et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Inhibitory, But Not Excitatory Synapses Are Reduced in the Hippocampus of the Six-Month-Old Alzheimer’s Disease Model Mouse

Pubblicato online: 01 mag 2023

Pagine: -

Ricevuto: 06 mar 2023

Accettato: 05 apr 2023

DOI: https://doi.org/10.2478/sjecr-2023-0003

Parole chiaveAlzheimer’s disease, hippocampus, GABAergic interneurons, synapses, vesicular transmitter transporters

© 2023 Miljana Aksic et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Parole chiave
Alzheimer’s disease, hippocampus, GABAergic interneurons, synapses, vesicular transmitter transporters