## 3 Results
### Vitamin Supplementation in AD  
The use of vitamin supplementation could play a key role in the management of AD-associated symptoms, helping to improve patients' quality of life [22; 23]. \begin{table}
\begin{tabular}{l l c} \hline \hline
**Item** & **Description** & **Maximum Points** \\ \hline \multirow{4}{*}{Randomization} & 1 point if randomization is mentioned. & \\  & 1 additional point if the method of randomization is appropriate. & \\  & Deduct 1 point if the method of randomization is inappropriate & 2 \\  & (minimum 0). & \\ \hline \multirow{4}{*}{Blinding} & 1 point if blinding is mentioned. & \\  & 1 additional point if the method of blinding is appropriate. & \\  & Deduct 1 point if the method of blinding is inappropriate & 2 \\  & (minimum 0). & \\ \hline \multirow{2}{*}{An account of all patients} & The fate of all patients in the trial is known. If there are no data, & 1 \\  & the reason is stated. & \\ \hline \hline \end{tabular}
\end{table} 
Table 1: Items and score of the standardized Jadad scale [21] used for reporting the quality of RCTs included in this systematic review. Figure 1: The PRISMA algorithm in this study. Table 2 shows the results of RCTs conducted on AD patients treated with vitamins of groups B, D, and E, administered alone or in combination. Group B vit, such as vitamin B9 (folic acid), B12 (cobalamin), and B6 (pyridoxine, pyridoxal, and pyridoxamine), are widely recognized for their potential to prevent the onset of AD and preserve cognitive function in patients with established disease [24]. As elevated homocysteine (Hcy) levels (over 12 umol/L) have been associated with an increased risk of cognitive decline and are very common in AD patients [6], the beneficial effects of these vitamins are related to their ability to reduce Hcy concentrations [25; 26]. Indeed, several studies [26; 27; 28; 29] have reported a reduction in Hcy levels in patients treated with vitamin B complex supplements. In particular, the daily use of 5 mg of folic acid, 25 mg of vitamin B6, and 1 mg of vitamin B12 was effective in providing a 7% reduction in plasma Hcy levels in the treated group compared with the placebo (\(p<0.001\)) [26]. [PERSON] et al. highlighted that the administration of 500 ug of mecobalamin (an isoform of vitamin B12), together with a complex containing 60 mg of iron, 5 mg of vitamin B6, 1 mg of folic acid, 10 mg of nicotinamide, 250 mg of calcium carbonate, 3 mg of thiamine mononitrate, 2 mg of riboflavin, 1 mg of calcium pantothenate, 100 ug of ascorbic acid, 100 ug of iodine, 150 ug of copper, 4000 IU of vitamin A, and 400 IU of vitamin D3 induced an average decrease of 2.25 umol/L (\(p=0.008\)) of Hcy concentration [27]. Similarly, [PERSON] et al. [28] found that over a period of 12 months supplementation with 1.2 mg of folic acid and 50 ug of vitamin B12 per day significantly increased the S-adenosyl-methionine (SAM)/S-adenosyl-homocysteine (SAH) ratio (\(p<0.001\)) with a consequent reduction in Hcy levels. However, it should be noted that the studies by [PERSON] et al. and [PERSON] et al. [26; 27], which utilized the same treatment albeit at different dosages, showed important safety issues in the supplemented group compared to the placebo group. [PERSON] et al. reported a higher rate of a depressed mood, depressive episodes, and established depression [26]; [PERSON] et al. reported a higher rate of delirium [27]. As vitamin D regulates key processes in the hippocampus, hypothalamus, and cortex [30], maintaining adequate levels of vitamin D is crucial for central nervous system (CNS) function, helping to prevent neuronal cell apoptosis, reducing synaptic degeneration, and modulating inflammation. This neuroprotective role is the main reason why vitamin D supplementation could help to slow AD progression [31]. The study by [PERSON] et al.