Background: Vitamin D deficiency and altered body composition are common in Alzheimer’s disease (AD). Memantine with vitamin D supplementation can protect cortical axons against amyloid-β exposure and glutamate toxicity. Objective: To study the effects of vitamin D deprivation and subsequent treatment with memantine and vitamin D enrichment on whole-body composition using a mouse model of AD. Methods: Male APPswe/PS1dE9 mice were divided into four groups at 2.5 months of age: the control group (n = 14) was fed a standard diet throughout; the remaining mice were started on a vitamin D-deficient diet at month 6. The vitamin D-deficient group (n = 14) remained on the vitamin D-deficient diet for the rest of the study. Of the remaining two groups, one had memantine (n = 14), while the other had both memantine and 10 IU/g vitamin D (n = 14), added to their diet at month 9. Serum 25(OH)D levels measured at months 6, 9, 12, and 15 confirmed vitamin D levels were lower in mice on vitamin D-deficient diets and higher in the vitamin D-supplemented mice. Micro-computed tomography was performed at month 15 to determine whole-body composition. Results: In mice deprived of vitamin D, memantine increased bone mineral content (8.7% increase, p <  0.01) and absolute skeletal tissue mass (9.3% increase, p <  0.05) and volume (9.2% increase, p <  0.05) relative to controls. This was not observed when memantine treatment was combined with vitamin D enrichment. Conclusion: Combination treatment of vitamin D and memantine had no negative effects on body composition. Future studies should clarify whether vitamin D status impacts the effects of memantine treatment on bone physiology in people with AD.

Acute pancreatitis (AP) is a common medical condition with a wide variety of etiologies. One of the common but frequently undetected causes of acute pancreatitis is microlithiasis, which can appear as biliary "sludge" in the gallbladder on imaging. While a broad workup should be initiated, endoscopic retrograde cholangiopancreatography (ERCP) is the gold standard for the diagnosis of microlithiasis. In this case, we present a severe presentation of acute pancreatitis in a teenager within the postpartum period. A 19-yearold woman presented with severe 10 out of 10 right upper quadrant (RUQ) pain with episodes of nausea that radiated to her back. She had no history of chronic alcoholism, illicit drug use, or over-the-counter supplement use, and no familial history of autoimmune disease, or pancreatitis. The patient was diagnosed with necrotizing acute pancreatitis with gallbladder "sludge" using contrast-enhanced computed tomography (CT) and magnetic resonance cholangiopancreatography (MRCP). She followed up with gastroenterology and had a great clinical recovery. Therefore, it is important to consider acute pancreatitis in patients with idiopathic pancreatitis in their postpartum period as they are prone to forming gallbladder "sludge" which can precipitate and cause a variation in gallbladder pancreatitis which can be difficult to detect on imaging.

Background Vitamin D (vitD) deficiency and changes in body composition are frequently observed in Alzheimer’s disease (AD). The combination of memantine and vitD has been shown to protect cortical axons from glutamate toxicity and beta‐amyloid in AD. Further to these central effects, vitD and memantine may act peripherally to alter metabolism. The purpose of this study was to assess changes in body composition (lean, adipose, and skeletal tissue) in an AD mouse model due to vitD deprivation and subsequent treatment with memantine and memantine combined with high dose vitD supplementation. Method Male APP/PS1 mice were randomized into four groups. Controls (n=14) received a standard diet throughout. The other three groups started a vitD deficient diet at month 6. At month 9, the VitD‐ group (n=14) remained on this diet, while the Mem&VitD‐ group (n=14) had memantine added, and the Mem&VitD+ group (n=14) had both memantine and 10 IU/g vitD added to their diet. Serum 25(OH)D3 levels were measured at months 6, 9, 12 and 15. Micro‐computed tomography scans were acquired at month 15 and segmented based on signal‐intensity to measure lean, adipose, and skeletal tissue mass and volume. Result Serum 25(OH)D3 measurements confirmed that mice on vitD‐deficient diets had lower levels (89% decrease), and mice on the vitD‐enriched diet (Mem&VitD+) had higher levels (129% increase), of 25(OH)D3 relative to mice on the standard diet. No differences were observed in adipose or lean tissue mass and volume between the four groups, however, there was a significant increase in skeletal tissue mass (9.3% increase, p<0.05) and volume (9.2% increase, p<0.05), and bone mineral content (8.7% increase, p<0.01) in the Mem&VitD‐ group relative to controls. Conclusion While vitD deprivation did not affect body composition in APP/PS1 mice at 15 months, memantine increased absolute skeletal tissue in mice that were vitD‐deficient. However, memantine did not have this effect in mice that were vitD‐enriched. We conclude that combination treatment of memantine and vitD enrichment had no negative effects on body composition in the APP/PS1 mouse model. Future work should clarify whether vitD status impacts the effects of memantine on bone physiology in people with AD.