{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,25]],"date-time":"2026-10-25T19:30:21Z","timestamp":1792956621625,"version":"4.5.0"},"reference-count":56,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2022,9,27]],"date-time":"2022-09-27T00:00:00Z","timestamp":1664236800000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAD"],"published-print":{"date-parts":[[2022,9,27]]},"abstract":"<jats:p>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\u2019s disease (AD) mouse models and previous clinical trials. Thus, although undetermined, MKP may be effective against pathological amyloid-\u03b2 (A\u03b2) accumulation-induced cognitive impairment. Objective: The current study aimed to investigate the potential of MKP as a pharmaceutical against AD by examining MKP\u2019s 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\u200a=\u200a38) with a C57BL\/6 background. A novel object recognition test was used to evaluate recognition memory. ELISA was used to measure insoluble A\u03b240, A\u03b242, and TNF-\u03b1 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 A\u03b240, A\u03b242, and TNF-\u03b1 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 A\u03b2 accumulation-induced cognitive impairment in APP\/PS1 mice. Furthermore, our findings suggest that MKP potentially contributes to preventing cognitive decline in AD.<\/jats:p>","DOI":"10.3233\/jad-220192","type":"journal-article","created":{"date-parts":[[2022,8,9]],"date-time":"2022-08-09T11:02:27Z","timestamp":1660042947000},"page":"835-848","source":"Crossref","is-referenced-by-count":6,"title":["Pharmaceutical Potential of Casein-Derived Tripeptide Met-Lys-Pro: Improvement in Cognitive Impairments and Suppression of Inflammation in APP\/PS1 Mice"],"prefix":"10.1177","volume":"89","author":[{"given":"Asuka","family":"Matsuzaki Tada","sequence":"first","affiliation":[{"name":"Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Japan"},{"name":"Functional Food Ingredients Research Section, Food Ingredients and Technology Institute, R&D Division, Morinaga Milk Industry Co., Ltd., Zama, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hamizah Shahirah","family":"Hamezah","sequence":"additional","affiliation":[{"name":"Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Japan"},{"name":"Institute of Systems Biology (INBIOSIS), Universiti Kebangsaan Malaysia, UKM Bangi, Selangor, Malaysia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aslina","family":"Pahrudin Arrozi","sequence":"additional","affiliation":[{"name":"Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zulzikry Hafiz","family":"Abu Bakar","sequence":"additional","affiliation":[{"name":"Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daijiro","family":"Yanagisawa","sequence":"additional","affiliation":[{"name":"Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ikuo","family":"Tooyama","sequence":"additional","affiliation":[{"name":"Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","reference":[{"key":"10.3233\/JAD-220192_ref3","doi-asserted-by":"crossref","first-page":"280","DOI":"10.1016\/j.jalz.2011.03.003","article-title":"Toward defining the preclinical stages of Alzheimer\u2019s disease: Recommendations from the National Institute on Aging-Alzheimer\u2019s Association workgroups on diagnostic guidelines for Alzheimer\u2019s disease","volume":"7","author":"Sperling","year":"2011","journal-title":"Alzheimers Dement"},{"key":"10.3233\/JAD-220192_ref4","doi-asserted-by":"crossref","first-page":"672","DOI":"10.1038\/360672a0","article-title":"Mutation of the beta-amyloid precursor protein in familial Alzheimer\u2019s disease increases beta-protein production","volume":"360","author":"Citron","year":"1992","journal-title":"Nature"},{"key":"10.3233\/JAD-220192_ref5","first-page":"2209","article-title":"The amyloid hypothesis of Alzheimer\u2019s disease: Progress and problems on the road to therapeutics","volume":"297","author":"Hardy","year":"2002","journal-title":"Erratum in: Science"},{"key":"10.3233\/JAD-220192_ref6","doi-asserted-by":"crossref","first-page":"181","DOI":"10.1016\/j.neuron.2004.09.010","article-title":"Deciphering the molecular basis of memory failure in Alzheimer\u2019s disease","volume":"44","author":"Walsh","year":"2004","journal-title":"Neuron"},{"key":"10.3233\/JAD-220192_ref7","doi-asserted-by":"crossref","first-page":"292","DOI":"10.1016\/j.pharmthera.2008.08.009","article-title":"AT2 receptors: Functional relevance in cardiovascular disease","volume":"120","author":"Jones","year":"2008","journal-title":"Pharmacol Ther"},{"key":"10.3233\/JAD-220192_ref8","doi-asserted-by":"crossref","first-page":"901","DOI":"10.1016\/S1357-2725(02)00306-0","article-title":"The brain renin-angiotensin system: Location and physiological roles","volume":"35","author":"McKinley","year":"2003","journal-title":"Int J Biochem Cell Biol"},{"key":"10.3233\/JAD-220192_ref9","doi-asserted-by":"crossref","first-page":"133","DOI":"10.1007\/s00424-012-1102-2","article-title":"The brain renin-angiotensin system: A diversity of functions and implications for CNS diseases","volume":"465","author":"Wright","year":"2013","journal-title":"Pflugers Arch"},{"key":"10.3233\/JAD-220192_ref10","doi-asserted-by":"crossref","first-page":"148","DOI":"10.1016\/j.mce.2008.11.003","article-title":"NADPH oxidases and angiotensin II receptor signaling","volume":"302","author":"Garrido","year":"2009","journal-title":"Mol Cell Endocrinol"},{"key":"10.3233\/JAD-220192_ref11","doi-asserted-by":"crossref","first-page":"2911","DOI":"10.1096\/fj.11-182873","article-title":". 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