Literature DB >> 35964178

Pharmaceutical Potential of Casein-Derived Tripeptide Met-Lys-Pro: Improvement in Cognitive Impairments and Suppression of Inflammation in APP/PS1 Mice.

Asuka Matsuzaki Tada1,2, Hamizah Shahirah Hamezah1,3, Aslina Pahrudin Arrozi1, Zulzikry Hafiz Abu Bakar1, Daijiro Yanagisawa1, Ikuo Tooyama1.   

Abstract

BACKGROUND: Tripeptide Met-Lys-Pro (MKP), a component of casein hydrolysates, has effective angiotensin-converting enzyme (ACE) inhibitory activity. Brain angiotensin II enzyme activates the NADPH oxidase complex via angiotensin II receptor type 1 (AT1) and enhances oxidative stress injury. ACE inhibitors improved cognitive function in Alzheimer's disease (AD) mouse models and previous clinical trials. Thus, although undetermined, MKP may be effective against pathological amyloid-β (Aβ) accumulation-induced cognitive impairment.
OBJECTIVE: The current study aimed to investigate the potential of MKP as a pharmaceutical against AD by examining MKP's effect on cognitive function and molecular changes in the brain using double transgenic (APP/PS1) mice.
METHODS: Experimental procedures were conducted in APP/PS1 mice (n = 38) with a C57BL/6 background. A novel object recognition test was used to evaluate recognition memory. ELISA was used to measure insoluble Aβ40, Aβ42, and TNF-α levels in brain tissue. Immunohistochemical analysis allowed the assessment of glial cell activation in MKP-treated APP/PS1 mice.
RESULTS: The novel object recognition test revealed that MKP-treated APP/PS1 mice showed significant improvement in recognition memory. ELISA of brain tissue showed that MKP significantly reduced insoluble Aβ40, Aβ42, and TNF-α levels. Immunohistochemical analysis indicated the suppression of the marker for microglia and reactive astrocytes in MKP-treated APP/PS1 mice.
CONCLUSION: Based on these results, we consider that MKP could ameliorate pathological Aβ accumulation-induced cognitive impairment in APP/PS1 mice. Furthermore, our findings suggest that MKP potentially contributes to preventing cognitive decline in AD.

Entities:  

Keywords:  APP/PS1 mice; Alzheimer’s disease; MKP; Met-Lys-Pro; dementia; peptide

Mesh:

Substances:

Year:  2022        PMID: 35964178      PMCID: PMC9535549          DOI: 10.3233/JAD-220192

Source DB:  PubMed          Journal:  J Alzheimers Dis        ISSN: 1387-2877            Impact factor:   4.160


  55 in total

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Journal:  Food Chem       Date:  2014-09-28       Impact factor: 7.514

6.  Effects of prolonged angiotensin-converting enzyme inhibitor treatment on amyloid beta-protein metabolism in mouse models of Alzheimer disease.

Authors:  Matthew L Hemming; Dennis J Selkoe; Wesley Farris
Journal:  Neurobiol Dis       Date:  2007-01-25       Impact factor: 5.996

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Journal:  FASEB J       Date:  2011-05-18       Impact factor: 5.191

8.  ACE inhibition with captopril retards the development of signs of neurodegeneration in an animal model of Alzheimer's disease.

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9.  Human astrocytes: secretome profiles of cytokines and chemokines.

Authors:  Sung S Choi; Hong J Lee; Inja Lim; Jun-ichi Satoh; Seung U Kim
Journal:  PLoS One       Date:  2014-04-01       Impact factor: 3.240

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