Neural stem cell transplantation improves learning and memory by protecting cholinergic neurons and restoring synaptic impairment in an amyloid precursor protein/presenilin 1 transgenic mouse model of Alzheimer's disease

Alzheimer's disease (AD) is the most prevalent age‑related neurodegenerative disorder. It is featured by the progressive accumulation of β‑amyloid (Aβ) plaques and neurofibrillary tangles. This can eventually lead to a decrease of cholinergic neurons in the basal forebrain. Stem cell transplant...

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Veröffentlicht in:Molecular medicine reports 2020-03, Vol.21 (3), p.1172-1180
Hauptverfasser: Zhu, Qing, Zhang, Nianping, Hu, Nan, Jiang, Rongrong, Lu, Huicong, Xuan, Aiguo, Long, Dahong, Chen, Yan
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container_title Molecular medicine reports
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creator Zhu, Qing
Zhang, Nianping
Hu, Nan
Jiang, Rongrong
Lu, Huicong
Xuan, Aiguo
Long, Dahong
Chen, Yan
description Alzheimer's disease (AD) is the most prevalent age‑related neurodegenerative disorder. It is featured by the progressive accumulation of β‑amyloid (Aβ) plaques and neurofibrillary tangles. This can eventually lead to a decrease of cholinergic neurons in the basal forebrain. Stem cell transplantation is an effective treatment for neurodegenerative diseases. Previous studies have revealed that different types of stem or progenitor cells can mitigate cognition impairment in different Alzheimer's disease mouse models. However, understanding the underlying mechanisms of neural stem cell (NSC) therapies for AD requires further investigation. In the present study, the effects and the underlying mechanisms of the treatment of AD by NSCs are reported. The latter were labelled with the enhanced green fluorescent protein (EGFP) prior to implantation into the bilateral hippocampus of an amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic (Tg) mouse model of AD. It was observed that the number of basal forebrain cholinergic neurons was restored and the expression of choline acetyltransferase (ChAT) protein was increased. Moreover, the levels of synaptophysin (SYP), postsynaptic density protein 95 (PSD‑95) and microtubule‑associated protein (MAP‑2) were significantly increased in the hippocampus of NSC‑treated AD mice. Notably, spatial learning and memory were both improved after transplantation of NSCs. In conclusion, the present study revealed that NSC transplantation improved learning and memory functions in an AD mouse model. This treatment allowed repairing of basal forebrain cholinergic neurons and increased the expression of the cognition‑related proteins SYP, PSD‑95 and MAP‑2 in the hippocampus.
doi_str_mv 10.3892/mmr.2020.10918
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It is featured by the progressive accumulation of β‑amyloid (Aβ) plaques and neurofibrillary tangles. This can eventually lead to a decrease of cholinergic neurons in the basal forebrain. Stem cell transplantation is an effective treatment for neurodegenerative diseases. Previous studies have revealed that different types of stem or progenitor cells can mitigate cognition impairment in different Alzheimer's disease mouse models. However, understanding the underlying mechanisms of neural stem cell (NSC) therapies for AD requires further investigation. In the present study, the effects and the underlying mechanisms of the treatment of AD by NSCs are reported. The latter were labelled with the enhanced green fluorescent protein (EGFP) prior to implantation into the bilateral hippocampus of an amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic (Tg) mouse model of AD. It was observed that the number of basal forebrain cholinergic neurons was restored and the expression of choline acetyltransferase (ChAT) protein was increased. Moreover, the levels of synaptophysin (SYP), postsynaptic density protein 95 (PSD‑95) and microtubule‑associated protein (MAP‑2) were significantly increased in the hippocampus of NSC‑treated AD mice. Notably, spatial learning and memory were both improved after transplantation of NSCs. In conclusion, the present study revealed that NSC transplantation improved learning and memory functions in an AD mouse model. 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It is featured by the progressive accumulation of β‑amyloid (Aβ) plaques and neurofibrillary tangles. This can eventually lead to a decrease of cholinergic neurons in the basal forebrain. Stem cell transplantation is an effective treatment for neurodegenerative diseases. Previous studies have revealed that different types of stem or progenitor cells can mitigate cognition impairment in different Alzheimer's disease mouse models. However, understanding the underlying mechanisms of neural stem cell (NSC) therapies for AD requires further investigation. In the present study, the effects and the underlying mechanisms of the treatment of AD by NSCs are reported. The latter were labelled with the enhanced green fluorescent protein (EGFP) prior to implantation into the bilateral hippocampus of an amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic (Tg) mouse model of AD. 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subjects Acetyltransferase
Advertising executives
Age
Alzheimer's disease
Amyloid beta-protein
Amyloid precursor protein
Animal cognition
Animal models
Basal forebrain
Brain
Brain research
Choline
Choline O-acetyltransferase
Cognition
Diseases
Epidermal growth factor
Experiments
Fibroblasts
Fluorescence
Forebrain
Genetic engineering
Green fluorescent protein
Hippocampus
Immunoglobulins
Medical research
Memory
Neural stem cells
Neurodegenerative diseases
Neurofibrillary tangles
Neurons
Postsynaptic density
Postsynaptic density proteins
Proteins
Rodents
Scientific equipment industry
Senile plaques
Spatial discrimination learning
Stem cell transplantation
Stem cells
Transgenic animals
Transgenic mice
Transplantation
β-Amyloid
title Neural stem cell transplantation improves learning and memory by protecting cholinergic neurons and restoring synaptic impairment in an amyloid precursor protein/presenilin 1 transgenic mouse model of Alzheimer's disease
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