CLSPCOL rescues Alzheimer’s disease mouse models
Abstract: Calmodulin-like skin protein (CLSP) inhibits Alzheimer’s disease (AD)-related neurotoxicity. The activity of CLSP is reduced in AD. To restore the CLSP activity, we developed a hybrid peptide named CLSPCOL, consisting of CLSP (1–61) and the collagen-homologous region (COL) of adiponectin. It was previously shown that the CLSPCOL-mediated restoration of the reduced CLSP activity alleviated memory impairment and neuronal synaptic loss in APPswe/PS1dE9 double transgenic mice (APP/PS1 mice) at an advanced phase. Here, we examined whether CLSPCOL is effective against the memory impairment of the APP/PS1 mice at an early phase, and the memory impairment, caused by the temporal disturbance of the cholinergic neurotransmission, that mimics a part of AD-linked neuronal abnormality. The CLSPCOL-mediated restoration of the CLSP activity corrected the impairment in acquisition of fear-conditioned memory at an early-phase AD model. A single subcutaneous injection of CLSPCOL rescued the short-term working memory impairment, caused by subcutaneous injection of scopolamine. We have concluded that CLSPCOL is a promising disease-modifying therapeutic agent for not only the advanced phase but also the early-phase AD. It also serves as a symptomatic modifier of AD by potentiating the cholinergic neurotransmission.
- Standort
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Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
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Online-Ressource
- Sprache
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Englisch
- Erschienen in
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CLSPCOL rescues Alzheimer’s disease mouse models ; volume:13 ; number:1 ; year:2022 ; pages:11-19 ; extent:9
Translational Neuroscience ; 13, Heft 1 (2022), 11-19 (gesamt 9)
- Urheber
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Kusakari, Shinya
Nawa, Mikiro
Hashimoto, Yuichi
Matsuoka, Masaaki
- DOI
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10.1515/tnsci-2022-0209
- URN
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urn:nbn:de:101:1-2022071914071160360112
- Rechteinformation
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
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15.08.2025, 07:27 MESZ
Datenpartner
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Kusakari, Shinya
- Nawa, Mikiro
- Hashimoto, Yuichi
- Matsuoka, Masaaki
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