Citrulline supplementation improves spatial memory in a murine model for Alzheimer's disease
Autor: | Paola Garcia-delaTorre, Eduardo Almeida-Gutiérrez, Katia Martínez-González, Juan Manuel Mejía-Aranguré, Salvador Flores-Chavez, Leonor Serrano-Cuevas |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Male medicine.medical_specialty Arginine Nutritional Supplementation Endocrinology Diabetes and Metabolism Morris water navigation task Hippocampus 030209 endocrinology & metabolism Mice Transgenic 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Oral administration Alzheimer Disease Internal medicine Memory improvement medicine Citrulline Animals Humans Cognitive decline Maze Learning Spatial Memory 030109 nutrition & dietetics Nutrition and Dietetics business.industry Disease Models Animal Endocrinology chemistry Dietary Supplements Female business |
Zdroj: | Nutrition (Burbank, Los Angeles County, Calif.). 90 |
ISSN: | 1873-1244 |
Popis: | Objectives Alzheimer's disease (AD) correlates with the dysfunction of metabolic pathways that translates into neurological symptoms. An arginine deficiency, a precursor of nitric oxide (NO), has been reported for patients with AD. We aimed to evaluate the effect of citrulline oral supplementation on cognitive decline in an AD murine model. Methods Three-month citrulline or water supplementation was blindly given to male and female wild-type and 3 × Tg mice with AD trained and tested in the Morris water maze. Cerebrospinal fluid and brain tissue were collected. Ultra-performance liquid chromatography was used for arginine determinations and the Griess method for NO. Results Eight-month-old male 3 × Tg mice with AD supplemented with citrulline performed significantly better in the Morris water maze task. Arginine levels increased in the cerebrospinal fluid although no changes were seen in brain tissue and only a tendency of increase of NO was observed. Conclusions Citrulline oral administration is a viable treatment for memory improvement in the early stages of AD, pointing to NO as a viable, efficient target for memory dysfunction in AD. |
Databáze: | OpenAIRE |
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