Abstract
In addition to D-Glucose, D-Ribose is also abnormally elevated in the urine of type 2 diabetic patients, establishing a positive correlation between the concentration of uric D-Ribose and the severity of diabetes. Intraperitoneal injection of D-Ribose causes memory loss and brain inflammation in mice. To simulate a chronic progression of age-related cognitive impairment, we orally administered D-Ribose by gavage at both a low and high dose to 8 week-old male C57BL/6J mice daily for a total of 6 months, followed by behavioral, histological and biochemical analysis. We found that long-term oral administration of D-Ribose impairs spatial learning and memory, accompanied by anxiety-like behavior. Tau was hyperphosphorylated at AT8, S396, S214 and T181 in the brain. Aβ-like deposition was also found in the hippocampus for the high dose group. D-Glucose-gavaged mice did not show significant memory loss and anxiety-like behavior under the same experimental conditions. These results demonstrate that a long-term oral administration of D-Ribose not only induces memory loss with anxiety-like behavior, but also elevates Aβ-like deposition and Tau hyperphosphorylation, presenting D-Ribose-gavaged mouse as a model for age-related cognitive impairment and diabetic encephalopathy.
Highlights
Alzheimer’s disease (AD), at times referred to as type 3 diabetes, is the most common form of dementia in elderly people [1]
We showed that feeding D-Ribose daily through gavage to mice for 6 months is correlated with cognitive impairment
Mice treated with D-Ribose (3.75 g/kg·d) exhibited learning and memory decline and anxiety-like behavior, accompanied by amyloid- β (Aβ)-like deposition and Tau hyperphosphorylation in their brain, especially the hippocampus
Summary
Alzheimer’s disease (AD), at times referred to as type 3 diabetes, is the most common form of dementia in elderly people [1]. AD patients suffer from memory loss, and other symptoms such as anxiety and depression [3]. Studies show that 25-60% of AD outpatients display anxiety symptoms. In particular transgenic mouse models, have been established to study memory loss, such as amyloid- β (Aβ)-depositing APP-transgenic [5] and APP/PS1transgenic mice [6], neurofibrillary tangle-forming P301L Tau transgenic mice [7], and the senescence accelerated mouse-prone 8 strain (SAMP8) [8]. When the Tau and Aβ pathology are combined in triple transgenic mice (3xTgAD), they display memory loss, anxiety-like behavior and subdued social behavior [9]. The Tg-APP (Sw, V717F)/B6 www.impactjournals.com/oncotarget mouse displays memory loss, anxiety-like behavior and decreased motor coordination [10]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
