Effects of GrandFusion Diet on Cognitive Impairment in Transgenic Mouse Model of Alzheimer’s Disease
Autor: | Cheryl L. Kirstein, Jin Yu, Hong Zhu, Stephen Perry, Mark S. Kindy, Saeid Taheri, William Mondy |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Male
0301 basic medicine Genetically modified mouse medicine.medical_specialty Time Factors Amyloid Traumatic brain injury Mice Transgenic Plaque Amyloid Inflammation lcsh:TX341-641 Article Cathepsin B Pathogenesis Mice 03 medical and health sciences 0302 clinical medicine Alzheimer Disease Internal medicine Nerve Growth Factor Presenilin-1 medicine Animals Humans Memory Disorders Amyloid beta-Peptides Nutrition and Dietetics business.industry behavior Brain amyloid medicine.disease Disease Models Animal Chronic traumatic encephalopathy 030104 developmental biology Endocrinology Nerve growth factor inflammation Female medicine.symptom business diet Alzheimer’s disease lcsh:Nutrition. Foods and food supply 030217 neurology & neurosurgery Food Science |
Zdroj: | Nutrients, Vol 13, Iss 117, p 117 (2021) Nutrients Volume 13 Issue 1 |
ISSN: | 2072-6643 |
Popis: | Alzheimer&rsquo s disease (AD) is the result of the deposition of amyloid &beta (A&beta ) peptide into amyloid fibrils and tau into neurofibrillary tangles. At the present time, there are no possible treatments for the disease. We have recently shown that diets enriched in phytonutrients show protection or limit the extent of damage in a number of neurological disorders. GrandFusion (GF) diets have attenuated the outcomes in animal models of traumatic brain injury, cerebral ischemia, and chronic traumatic encephalopathy. In this study, we investigated the effect of GF diets in a mouse model of AD prior to the development of amyloid plaques to show how this treatment paradigm would alter the accumulation of A&beta peptide and related pathologic changes (i.e., inflammation, cathepsin B, and memory impairment). Administration of GF diets (2&ndash 4%) over a period of four months in APP/&Delta PS1 double-transgenic mice resulted in attenuation in A&beta peptide levels, reduction of amyloid load, and inflammation, increased cathepsin B expression, and improved spatial orientation. Additionally, treatment with GF diets increased nerve growth factor (NGF) levels in the brain and tempered the memory impairment in the animal model. These data suggest that GF diets may alter the development and progression of the mechanisms associated with the disease process to effectively modify AD pathogenesis. |
Databáze: | OpenAIRE |
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