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.

Location
Deutsche Nationalbibliothek Frankfurt am Main
Extent
Online-Ressource
Language
Englisch

Bibliographic citation
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)

Creator
Kusakari, Shinya
Nawa, Mikiro
Hashimoto, Yuichi
Matsuoka, Masaaki

DOI
10.1515/tnsci-2022-0209
URN
urn:nbn:de:101:1-2022071914071160360112
Rights
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Last update
15.08.2025, 7:27 AM CEST

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Associated

  • Kusakari, Shinya
  • Nawa, Mikiro
  • Hashimoto, Yuichi
  • Matsuoka, Masaaki

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