Calorie restriction (CR) is recognized for its potential to delay age-related changes; however, its effectiveness can vary based on factors such as duration, age, and sex. Implementing CR later in life may not only diminish its protective potential but could also have detrimental effects. Herein, we aimed to investigate the effect of CR on short-term (STM) and long-term (STM) memory and explore the potential role of the mTOR signaling pathway as an underlying molecular mechanism. Female Wistar rats of different ages (adult, middle-aged, and old) were exposed to CR (60% of ad libitum (AL)) to study the effect of CR at early (EOCR) and at late onset (LOCR). AL fed animals were used to test the effects of aging and as age-matched controls for the effect of CR. Memory assessments were conducted using the Novel Object Recognition Test (NORT), evaluating both STM and LTM. Western blot analysis was employed to assess the expression of key molecules within the mTOR signaling pathway in the rat hippocampus. At 18 months of age, STM was preserved in both EOCR and LOCR groups, while LTM was preserved only in EOCR rats. In 24-month-old females, LOCR worsened STM and LTM performances in comparison to the age matching AL controls. Correspondingly, phosphorylation of mTOR and AKT was increased in 24-month-old LOCR animals. While EOCR successfully preserved STM and LTM up to a certain point in life, LOCR appeared to worsen memory performance in older animals, possibly due to increased mTOR phosphorylation in the hippocampus.