Application of dimethyl mercaptopropionic acid

Abstract

The invention discloses application of dimethyl mercaptopropionic acid, and relates to the field of medicines. Specifically, the invention provides application of dimethyl mercaptopropionic acid in preparation of drugs for treating Alzheimer's disease. The dimethyl mercaptopropionic acid can reverse the change of the expression level of MAG, CD9 and P2ry12 proteins in the brain of an Alzheimer's disease model mouse, plays a role in remyelination protection and neural immune regulation and control, can reduce the expression level of Alzheimer's disease pathology-related proteins A beta and tau, and has a good application prospect. The spatial learning ability and the spatial memory ability of mice suffering from the Alzheimer disease are improved, and the alzheimer disease can be treated.

Description

Technical Field

[0001] The invention relates to the field of medicine, and in particular to an application of dimethylmercaptopropionic acid. Background Art

[0002] Neurodegeneration is a common feature of many brain diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). AD is an age-related neurodegenerative disease characterized by memory loss and cognitive decline. With the gradual aging of the world, AD is an increasingly serious public health problem. The pathogenesis of AD has always been the focus of scientists, but there is still no definite conclusion so far. The main pathological characteristics of AD are senile plaques formed by the deposition of extracellular β-amyloid protein (Aβ) and neurofibrillary tangles formed by the hyperphosphorylation of intracellular Tau protein, and a variety of hypotheses have been proposed based on this. The drugs that have been developed for these hallmark pathological features cannot prevent the progression of the disease even if they successfully reduce Aβ plaques.

[0003] In the central nervous system, myelin is a multilayer lipid structure wrapped around the axon, isolating the neuronal axon from the surrounding environment and allowing the action potential to propagate effectively along the axon. In addition to the classic amyloid hypothesis, myelin loss is also considered to be another key pathological feature of AD, and related proteins that maintain the integrity of myelin are significantly reduced in the brain tissue of AD patients. Recently, studies have suggested that Aducanumab, the only amyloid-targeted drug approved by the Food and Drug Administration (FDA), may be more effective when used in combination with drugs that target oligodendrocytes and promote myelin regeneration.

[0004] Dimethylsulphoniopropionate (DMSP) is a natural product widely distributed in the ocean. It is mainly produced by algae, corals, and bacteria, and serves as their osmotic agent, cryoprotectant, and antioxidant. In addition, DMSP is also an important component of the marine sulfur cycle. In addition to playing a role in natural biogeochemical processes, DMSP also has high biomedical research value. Studies have shown that DMSP can improve the antioxidant capacity of mammalian nerve cells, promote cell survival, and improve diseases such as breast cancer, induced diabetes, and Parkinson's disease. However, there are currently no reports documenting the use of DMSP in promoting myelin regeneration, nor has there been any report on the use of DMSP in the treatment of AD.

[0005] Therefore, the prior art still needs to be improved and developed. Summary of the invention

[0006] In view of the above-mentioned deficiencies in the prior art, the object of the present invention is to provide an application of dimethylmercaptopropionic acid, aiming to develop a drug for treating Alzheimer's disease.

[0007] The technical solution of the present invention is as follows:

[0008] The first aspect of the present invention provides the use of dimethylmercaptopropionic acid in the preparation of a drug for treating Alzheimer's disease.

[0009] The second aspect of the present invention provides the use of dimethylmercaptopropionic acid in the preparation of a medicament for treating myelin sheath damage.

[0010] The third aspect of the present invention provides the use of dimethylmercaptopropionic acid in the preparation of drugs for neuroimmune regulation.

[0011] Optionally, the drug includes dimethylmercaptopropionic acid, and at least one of a pharmaceutically acceptable carrier, a pharmaceutically acceptable excipient, a pharmaceutically acceptable adjuvant, and a pharmaceutically acceptable prodrug.

[0012] Optionally, the pharmaceutically acceptable carrier includes at least one of sugar, starch, and cellulose.

[0013] Optionally, the pharmaceutically acceptable excipients include at least one of a solvent, an excipient, a buffer, a lubricant, a colorant, a release agent, a coating agent, a flavoring agent, a preservative, and an antioxidant.

[0014] Optionally, the dosage form of the drug is selected from one of solution, pill, tablet, capsule, powder, lozenge, and paste.

[0015] Optionally, the administration route of the drug includes a combination of one or more of oral administration, intravenous injection, intraperitoneal injection, intramuscular injection, and subcutaneous injection.

[0016] Beneficial effects: The dimethylmercaptopropionic acid in the present invention can reverse the changes in the expression levels of MAG, CD9 and P2ry12 proteins in the brains of Alzheimer's disease model mice, and play a role in myelin regeneration protection and neuroimmune regulation. At the same time, dimethylmercaptopropionic acid can reduce the expression levels of Alzheimer's disease pathology-related proteins Aβ and tau, and improve the spatial learning ability and spatial memory ability of Alzheimer's disease mice, and can be used to treat Alzheimer's disease. BRIEF DESCRIPTION OF THE DRAWINGS

[0017] Figure 1 This is a comparison chart of the escape latency of each group of mice changing over time in Example 1 of the present invention.

[0018] Figure 2 This is a graph showing the time each group of mice stayed in the original platform quadrant during the 24-hour test in Example 1 of the present invention.

[0019] Figure 3 This is a graph showing the number of times each group of mice crossed the platform in the 24-hour test in Example 1 of the present invention.

[0020] Figure 4 This is a graph showing the time each group of mice stayed in the original platform quadrant during the 72-hour test in Example 1 of the present invention.

[0021] Figure 5 This is a graph showing the number of times each group of mice crossed the platform during the 72-hour test in Example 1 of the present invention.

[0022] Figure 6 This is a graph showing the relative expression levels of HT7 protein in the brains of each group of mice in Example 2 of the present invention.

[0023] Figure 7 This is a graph showing the relative expression levels of Tau-pS404 protein in the brains of each group of mice in Example 2 of the present invention.

[0024] Figure 8 This is a graph showing the relative expression levels of Aβ1-42 protein in the brains of each group of mice in Example 2 of the present invention.

[0025] Fig. 9 This is a graph showing the results of GO enrichment analysis of differentially expressed proteins between the DMSP (L) group and the AD group of mice in Example 3 of the present invention.

[0026] Fig.10 This is a graph showing the results of GO enrichment analysis of differentially expressed proteins between the DMSP (H) group and the AD group of mice in Example 3 of the present invention.

[0027] Fig.11 This is a graph showing the PPI network analysis results of the commonly differentially expressed proteins in the DMSP(L) / AD comparison group and the AD / WT comparison group in Example 3 of the present invention.

[0028] Fig.12 This is a graph showing the PPI network analysis results of the commonly differentially expressed proteins in the DMSP(H) / AD comparison group and the AD / WT comparison group in Example 3 of the present invention.

[0029] Fig.13 This is a graph showing the PPI network analysis results of the commonly differentially expressed proteins in the DMSP(L) / AD, DMSP(H) / AD and AD / WT comparison groups in Example 3 of the present invention.

[0030] Fig.14 This is a graph showing the relative expression of MAG protein in mouse hippocampal tissue in Example 4 of the present invention.

[0031] Fig.15This is a graph showing the relative expression of CD9 protein in mouse hippocampal tissue in Example 4 of the present invention.

[0032] Fig.16 This is a graph showing the relative expression of P2ry12 protein in mouse hippocampal tissue in Example 4 of the present invention. DETAILED DESCRIPTION

[0033] The present invention provides an application of dimethylmercaptopropionic acid. To make the purpose, technical solution and effect of the present invention clearer and more specific, the present invention is further described in detail below. It should be understood that the specific embodiments described herein are only used to explain the present invention and are not used to limit the present invention.

[0034] Unless otherwise defined, all technical terms and scientific terms used herein have the same meaning as those commonly understood by those skilled in the art of the present invention. The terms used in the specification of the present invention herein are only for the purpose of describing specific embodiments and are not intended to limit the present invention.

[0035] The embodiment of the present invention provides the use of dimethylmercaptopropionic acid in preparing a medicine for treating Alzheimer's disease.

[0036] The embodiment of the present invention also provides the use of dimethylmercaptopropionic acid in preparing a medicine for treating myelin sheath damage.

[0037] The embodiment of the present invention also provides the use of dimethylmercaptopropionic acid in preparing a drug for neuroimmune regulation.

[0038] In the embodiment of the present invention, dimethylmercaptopropionic acid can reverse the changes in the expression levels of MAG, CD9 and P2ry12 proteins in the brain of Alzheimer's disease model mice, play a role in myelin regeneration protection and neuroimmune regulation, and at the same time, dimethylmercaptopropionic acid can reduce the expression levels of Alzheimer's disease pathology-related proteins Aβ and tau, improve the spatial learning ability and spatial memory ability of Alzheimer's disease mice, and can be used to treat Alzheimer's disease. In addition, dimethylmercaptopropionic acid has a regulatory function on biological processes such as the physiological state of glial cells, myelination, axon guidance, complement system, cholinergic synapses and metal ion responses in the brain of Alzheimer's disease model mice.

[0039] In some embodiments, the drug includes dimethylmercaptopropionic acid (active ingredient), and at least one of a pharmaceutically acceptable carrier, a pharmaceutically acceptable excipient, a pharmaceutically acceptable adjuvant, and a pharmaceutically acceptable prodrug.

[0040] In some specific embodiments, the drug includes a therapeutically effective amount of dimethylmercaptopropionic acid, and at least one of a pharmaceutically acceptable carrier, a pharmaceutically acceptable excipient, a pharmaceutically acceptable adjuvant, and a pharmaceutically acceptable prodrug.

[0041] In this embodiment, the therapeutically effective amount refers to the dosage of the dimethylmercaptopropionic acid of the embodiment of the present invention that is sufficient to show benefit or clinical significance to an individual. It will be understood by those skilled in the art that the actual amount or dosage administered and the administration schedule will depend on the nature and severity of the disease being treated, the age and general condition of the subject being treated, and the mode of administration, etc.

[0042] In one embodiment, the pharmaceutically acceptable carrier includes one or more of sugar, starch, cellulose and their derivatives, but is not limited thereto.

[0043] In some specific embodiments, the sugar may be selected from at least one of lactose, glucose, and sucrose, but is not limited thereto; the starch may be selected from at least one of corn starch and potato starch, but is not limited thereto; the cellulose and its derivatives may be selected from at least one of sodium carboxymethyl cellulose, ethyl cellulose, and cellulose acetate, but is not limited thereto.

[0044] The pharmaceutically acceptable excipient refers to any excipient known to those skilled in the art that is suitable for a specific mode of administration, and the excipient should be non-toxic, not interfere with or impair the efficacy of the active ingredient of the embodiment of the present invention, and the excipient can be flexibly selected according to the specific dosage form of the drug described in the above embodiment. In one embodiment, the pharmaceutically acceptable excipient includes at least one of a pharmaceutically acceptable solvent, excipient, buffer, lubricant, colorant, release agent, coating agent, flavoring agent, preservative, and antioxidant, but is not limited thereto.

[0045] In a specific embodiment, the excipient includes one or more of cocoa butter, suppository wax, vegetable oil, alcohol, ester, and agar, but is not limited thereto.

[0046] In some embodiments, the vegetable oil is selected from at least one of peanut oil, cottonseed oil, safflower oil, sesame oil, olive oil, corn oil, and soybean oil, but is not limited thereto; the alcohol is selected from propylene glycol, but is not limited thereto; the ester is selected from at least one of ethyl oleate and ethyl dodecanoate, but is not limited thereto.

[0047] In a specific embodiment, the buffer includes one of magnesium hydroxide, aluminum hydroxide, alginic acid, pyrogen-free water, isotonic saline, Ringer's solution, ethanol and phosphate buffer solution, but is not limited thereto.

[0048] In one embodiment, the lubricant includes one or both of sodium lauryl sulfate and magnesium stearate, but is not limited thereto.

[0049] In one embodiment, the dosage form of the drug is selected from one of a solution, a pill, a tablet, a capsule, a powder, a lozenge, and a paste.

[0050] In one embodiment, the administration route of the drug includes a combination of one or more of oral administration, intravenous injection, intraperitoneal injection, intramuscular injection, and subcutaneous injection.

[0051] The following describes it in detail through specific embodiments.

[0052] In the following examples, Alzheimer's disease is referred to as AD, and dimethylmercaptopropionic acid is referred to as DMSP.

[0053] The present invention uses triple transgenic AD model mice (3×Tg-AD) as the research object, sets up different doses of DMSP administration groups, and analyzes the intervention effect and mechanism of DMSP on 3×Tg-AD mice. First, the spatial learning and memory ability of mice was evaluated by Morris water maze experiment, and then the relative expression of AD pathology-related proteins (Aβ and phosphorylated tau protein) in the brain of mice was detected by immunoblotting (Western-Blot), and then the proteomics study of DMSP-treated and untreated AD mice and wild-type (Wild-type, WT) mice hippocampal tissue was performed to further understand the mechanism of action of DMSP.

[0054] The DMSP used in the following examples was provided by Changchun Institute of Applied Chemistry.

[0055] The 3×Tg-AD and WT mice used in the following examples were purchased from Jackson Laboratory. These mice express mutant human APPswe and tauP301L genes and mutant mouse PS1M146V genes.

[0056] Four-month-old 3×Tg-AD mice were divided into DMSP(L) group, DMSP(H) group and AD control group (referred to as AD group), with 20 mice in each group, including 10 female mice and 10 male mice in each group. Among them, the DMSP(L) group was a low-dose DMSP administration group, and the DMSP(H) group was a high-dose DMSP administration group.

[0057] The DMSP (L) group was treated with 7 μg / mL DMSP added to the drinking water of mice for 12 weeks, and the DMSP (H) group was treated with 11 μg / mL DMSP added to the drinking water of mice for 12 weeks. Mice in the AD group received normal drinking water. At the same time, a WT control group (referred to as the WT group) of mice was set up, which also received normal drinking water. All mice were fed under standard conditions (the temperature in the animal room was maintained at 22±2°C, alternating day and night every 12 hours), and the feed was purchased from the Guangdong Medical Experimental Animal Center (Guangzhou, China). Specifically, the mouse groups are set as shown in Table 1.

[0058] Table 1. Mouse group settings

[0059]

[0060] Example 1 Evaluation of spatial learning and memory ability of mice by Morris water maze test

[0061] The mice in the WT, AD, DMSP(L) and DMSP(H) groups underwent training experiments in a circular pool (160 cm in diameter and 50 cm in height), which were mainly divided into two parts: positioning navigation experiment and space exploration experiment.

[0062] Positioning navigation experiment: Each mouse was trained 4 times a day for 5 consecutive days. The maximum test time for each mouse during each training was 60 seconds. During this period, the time required for the mouse to find the hidden platform was measured, which was the escape latency. A shorter escape latency was considered to have better spatial learning ability. If the mouse did not reach the platform within the specified time, it was manually guided to the platform and stayed there for 15 seconds. The results are as follows: Figure 1 As shown in the figure, the escape latency of AD mice was significantly longer than that of WT mice, indicating that the spatial learning ability of AD mice was impaired. However, the escape latency of DMSP (L) and DMSP (H) group mice showed that the escape latency of AD mice was shortened after DMSP treatment. One-way ANOVA showed that Figure 1 As shown, DMSP-treated AD mice performed significantly better than the AD group mice starting from the 3rd day and showed a significantly shortened total escape latency during 5 consecutive days of training, which indicates that DMSP can improve the spatial learning impairment of AD mice and enhance the spatial learning ability of AD mice.

[0063] Spatial exploration experiment: 24h and 72h after the last day of navigation training, spatial exploration experiments were conducted to evaluate the short-term and long-term memory of mice. The platform was removed and the mice were placed in the quadrant of the pool opposite to the original platform quadrant. Each mouse was allowed to swim for 60 seconds, and the time the mouse stayed in the original platform quadrant and the number of times the mouse crossed the platform position were recorded. The longer the time spent in the original platform quadrant and the more times the mouse crossed the platform position, the better the spatial memory ability was. Figure 2 and 3 As shown in the figure, 24 hours after the training, the time that the mice in the AD group stayed in the original platform quadrant and the number of times they crossed the platform position were significantly less than those in the WT group, but this phenomenon was significantly reversed after DMSP treatment. The time that the mice treated with DMSP stayed in the original platform quadrant and the number of times they crossed the platform position were significantly higher than those in the AD group. Figure 4 and 5 As shown in the figure, in the exploration experiment after 72 hours, the time that the mice in the DMSP (L) group stayed in the original platform quadrant was still significantly higher than that of the mice in the AD group. The above results indicate that DMSP can improve the spatial memory impairment of AD mice and enhance the spatial memory ability of AD mice.

[0064] in, Figure 1-Figure 5 In the above equation, the number of samples is n=10. # Indicates P < 0.05 compared between WT group and AD group; ## Indicates P < 0.01 compared with the WT group and the AD group; ### Indicates that P<0.001 was found between the WT group and the AD group; * indicates that P<0.05 was found between the drug-treated group and the AD group; ** indicates that P<0.01 was found between the drug-treated group and the AD group; *** indicates that P<0.001 was found between the drug-treated group and the AD group.

[0065] Example 2 Detection of typical AD pathological features in mouse brain

[0066] The main pathological features of AD are senile plaques formed by extracellular Aβ deposition and neurofibrillary tangles formed by hyperphosphorylation of intracellular Tau protein. Western-Blot was used to detect the relative expression levels of total tau, phosphorylated tau and Aβ proteins in the mouse brain. The results are as follows Figure 6-Figure 8 As shown (wherein, the number of samples n = 3; # Indicates P < 0.05 compared between WT group and AD group; ### Indicates P < 0.001 compared with the WT group and the AD group; #####=Indicates P<0.0001 compared with WT group and AD group; * indicates P<0.05 compared with drug-treated group and AD group; ** indicates P<0.01 compared with drug-treated group and AD group). The results of detecting the relative expression levels of total tau, phosphorylated tau and Aβ protein in the brain of mice showed that DMSP treatment could reduce the expression levels of HT7 and Tau-pS404 in the brain of AD mice and reduce the aggregation of Aβ1-42 in the brain of AD mice.

[0067] Example 3 Proteomic analysis of the hippocampal tissues of the DMSP (L) group, DMSP (H) group, AD group, and WT group mice was performed to understand the mechanism of action of DMSP

[0068] Data independent acquisition (DIA) proteomics was used to analyze the changes in protein expression levels in mouse hippocampal tissue. The left hippocampus of 8 mice (4 females + 4 males) was collected in each group, and then 2 mice of the same sex were randomly selected and combined into one sample, that is, 4 combined samples were obtained in each group. The total protein in the samples was extracted, and a part was taken out for protein concentration determination and sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) detection, and another part was taken for trypsin digestion. After desalting the enzymatic peptides, the samples were identified by LC-MS / MS. LC-MS / MS identification was divided into two main steps. The first step was to establish a protein spectrum library using the traditional data-dependent acquisition (DDA) method, and the second step was to use the data-independent acquisition (DIA) technology to collect mass spectrometry data for each sample. Spectral matching, quantitative information extraction and subsequent statistical analysis were performed based on the DDA database. The screening criteria for differentially expressed proteins (DEPs) were ≥1.2 or ≤0.83 and p value <0.05. After obtaining DEPs, GO enrichment analysis was performed on DEPs, and protein interaction (PPI) network analysis was performed on reversal proteins to describe the function of DMSP. GO generally includes three ontologies: biological process, cellular component, and molecular function. The -log10Pvalue (Pvalue is the P value) corresponding to each entry under each ontology was sorted from large to small, and the top 10 entries were selected to obtain the top 30 entries in GO enrichment analysis.

[0069] Three comparison groups were established by the above method: (i) DMSP(L) group mice were compared with AD group mice, namely DMSP(L) / AD comparison group; (ii) DMSP(H) group mice were compared with AD group mice, namely DMSP(H) / AD comparison group; (iii) AD group mice were compared with WT group mice, namely AD / WT comparison group. Figure 9-13 shown.

[0070] Compared with the AD group, 191 proteins were upregulated and 43 proteins were downregulated in the DMSP(L) group, and 100 proteins were upregulated and 46 proteins were downregulated in the DMSP(H) group. These DEPs were subjected to GO enrichment analysis. Fig. 9 and 10 As shown in the figure, DMSP causes significant changes in myelination, axon development, metal ion response and complement activation / alternative pathways in biological processes. The changes in cellular components caused by DMSP mainly include myelin, axon internode region, protein complexes involved in cell adhesion, endoplasmic reticulum membrane components and neuronal dense core vesicles. The effects of DMSP on molecular functions mainly include ubiquitin ligation, complement component C1q complex binding, structural components of myelin, insulin-like growth factor binding, zinc ion binding and the activity of enzymes related to post-translational modification (such as N-acetyltransferase activity, glycosyltransferase activity, protein serine / threonine phosphatase inhibitor activity, etc.).

[0071] Compared with the WT group, a total of 479 DEPs were identified in the AD group. The detection results of the two comparison groups DMSP(L) / AD and AD / WT contained 61 identical DEPs, of which 60 were reversal proteins. The PPI network analysis of reversal proteins showed the following results: Fig.11 As shown, the results showed that they were mainly involved in glial cell differentiation, myelination, axon guidance and complement pathways.

[0072] The detection results of the two comparison groups, DMSP(H) / AD and AD / WT, contained 44 identical DEPs, all of which were reversal proteins. The results of the reversal protein PPI network analysis were as follows: Fig.12 As shown in the figure, the results showed that they were mainly involved in myelination, axon guidance, cell connection and protein membrane localization. The detection results of the three comparison groups of DMSP(L) / AD, DMSP(H) / AD and AD / WT contained 20 identical DEPs, all of which were reversal proteins. The PPI network analysis of reversal proteins was shown in Fig.13 As shown, the results indicate that they are mainly involved in myelin formation, cell junctions, extracellular vesicles and axon guidance.

[0073] Example 4

[0074] Based on the results of proteomic analysis, both the low-dose DMSP treatment group and the high-dose DMSP treatment group showed effects on myelination, axon guidance and metal ion response, as shown in Table 2 Three reversal proteins, CD9, MAG and P2ry12, were selected based on the above PPI network analysis and verified by Western-Blot.

[0075] Table 2 Proteins whose expression levels in AD can be reversed by DMSP treatment and verified by WB according to PPI network analysis

[0076]

[0077]

[0078] Verification results such as Figure 14-16 (Wherein, the number of samples is n=3; ## Indicates that the WT group is compared with the AD group, P<0.01; * indicates that the drug-treated group is compared with the AD group, P<0.05; ** indicates that the drug-treated group is compared with the AD group, P<0.01; *** indicates that the drug-treated group is compared with the AD group, P<0.001). In addition to the classic amyloid β hypothesis and the tau protein hyperphosphorylation hypothesis, demyelination is also considered to be another key pathological feature of AD, which may occur before the development of amyloid pathology. Myelin-associated glycoprotein (MAG) is located in the innermost layer of the myelin membrane that is in direct contact with the axon. It participates in the formation of myelin and the maintenance of its integrity by mediating the interaction between glial cells and axons. CD9 antigen (CD9antigen, CD9) appears in the final stage of myelination formation. CD9 participates in the communication between axons and glial cells, and plays an important role in the formation of paranodal connections in the nodes of Ranvier. As Fig.14 and 15 As shown in the figure, compared with the WT group mice, the expression levels of MAG and CD9 in the hippocampus of the AD group mice decreased, and the expression levels of MAG and CD9 were increased after DMSP treatment, maintaining the integrity of the myelin sheath and helping the conduction of nerve impulses. Therefore, DMSP plays an important role in restoring myelin damage in the brain of AD mice, and can be used as a myelin regeneration protective agent for the treatment of myelin damage.

[0079] Microglia are the main immune cells in the central nervous system and play a key role in immune surveillance, synaptic pruning and clearance of abnormal proteins. P2Y purinoceptor 12 (P2ry12) is a purinergic receptor highly expressed in microglia in the brain and can be used as a marker for homeostatic microglia. Mice lacking this receptor show abnormalities in microglial migration and polarization. Fig.16As shown in the figure, compared with the WT group mice, the expression level of P2ry12 in the hippocampus of the AD group mice decreased. After DMSP treatment, the expression level of P2ry12 in the hippocampus of the AD mice was increased and the physiological state of microglia was stabilized. The above results show that DMSP can achieve neuroprotection by coordinating the state of microglia, and can be used as a neuroimmunomodulator for neuroimmune regulation. DMSP exerts anti-AD efficacy through the mechanism of action that plays a role in myelin regeneration protection and neuroimmune regulation.

[0080] Depend on Figure 14-16 The verification results of CD9, MAG and P2ry12 were consistent with the proteomics results.

[0081] In summary, the present invention provides an application of dimethylmercaptopropionic acid. In the present invention, dimethylmercaptopropionic acid can reverse the changes in the expression levels of MAG, CD9 and P2ry12 proteins in the brain of Alzheimer's disease model mice, and play a role in myelin regeneration protection and neuroimmune regulation. At the same time, dimethylmercaptopropionic acid can reduce the expression levels of Alzheimer's disease pathology-related proteins Aβ and tau, and improve the spatial learning ability and spatial memory ability of Alzheimer's disease mice, and can be used to treat Alzheimer's disease.

[0082] It should be understood that the application of the present invention is not limited to the above examples. For ordinary technicians in this field, improvements or changes can be made based on the above description. All these improvements and changes should fall within the scope of protection of the claims attached to the present invention.

Claims

1. Use of dimethylmercaptopropionic acid in the preparation of a drug for treating Alzheimer's disease.

2. Application of dimethylmercaptopropionic acid in the preparation of drugs for treating myelin sheath damage.

3. Application of dimethylmercaptopropionic acid in the preparation of drugs for neuroimmunomodulation.

4. The use according to any one of claims 1 to 3, characterized in that: The drug comprises dimethylmercaptopropionic acid and at least one of a pharmaceutically acceptable carrier, a pharmaceutically acceptable excipient, a pharmaceutically acceptable adjuvant, and a pharmaceutically acceptable prodrug.

5. The use according to claim 4, characterized in that: The pharmaceutically acceptable carrier includes at least one of sugar, starch and cellulose.

6. The use according to claim 4, characterized in that: The pharmaceutically acceptable excipients include at least one of solvents, excipients, buffers, lubricants, colorants, release agents, coating agents, flavoring agents, preservatives, and antioxidants.

7. The use according to claim 4, characterized in that: The dosage form of the drug is selected from one of solution, pill, tablet, capsule, powder, lozenge and paste.

8. The use according to claim 4, characterized in that: The administration route of the drug includes one or more combinations of oral administration, intravenous injection, intraperitoneal injection, intramuscular injection, and subcutaneous injection.

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