A pharmaceutical composition for preventing and adjuvant treating Alzheimer's disease and a preparation method thereof

Abstract

The present application relates to a kind of drug composition for preventing and adjuvant therapy of Alzheimer's disease and preparation method thereof, belong to medical health technical field.The prescription of the drug composition prepared in the present application includes the following active ingredients, phosphatidylserine, pyrrole quinoline quinone, coenzyme Q10, curcumin, EGCG, alpha-lipoic acid, acetyl L-carnitine, magnesium threonate, vitamin E, folic acid and vitamin B12.The preparation method of the drug composition also includes the following steps: the product is loaded with energy by weak magnetic resonance equipment to the composition.The drug composition reaches the effect of antioxidation, anti-inflammation, improves cerebral blood flow and protects neuron by the synergistic effect of multiple functional components, so as to help slow down the progress of Alzheimer's disease.

Description

Technical Field

[0001] This invention belongs to the field of pharmaceutical and health care technology, and relates to a pharmaceutical composition for the prevention and treatment of Alzheimer's disease and its preparation method. Background Technology

[0002] Alzheimer's disease (AD) is a common neurodegenerative disease, primarily characterized by memory loss, cognitive impairment, and behavioral abnormalities. Currently, there is no cure, and drug treatments have limited effectiveness and significant side effects. Recent studies have found that supplementing with specific functional ingredients (such as antioxidants and neuroprotective agents) can slow disease progression and improve symptoms. Therefore, developing a safe and effective health supplement formula is of great significance.

[0003] The relationship between Alzheimer's disease and mitochondria is an active area of ​​research. Mitochondria are the energy factories within cells, responsible for producing ATP (the main form of cellular energy) and playing a crucial role in cellular metabolism, oxidative stress, and cell death. Brain cells in Alzheimer's patients often exhibit impaired energy metabolism. Studies have found that mitochondrial function is damaged in the brain tissue of Alzheimer's patients, leading to insufficient energy production. This energy deficiency can affect the normal function of neurons, resulting in cognitive decline. Mitochondria are also a major source of oxidative stress. Elevated levels of oxidative stress are frequently found in the brain tissue of Alzheimer's patients, leading to cell damage and death. Mitochondrial dysfunction may lead to the excessive production of free radicals, thereby exacerbating oxidative stress and damaging neurons. Due to the importance of mitochondria in Alzheimer's disease, researchers are exploring therapeutic strategies targeting mitochondria. For example, certain drugs and supplements are being investigated to improve mitochondrial function, which may help slow the progression of Alzheimer's disease.

[0004] The pathogenesis of Alzheimer's disease is complex. Existing drug treatments, such as acetylcholinesterase inhibitors (donepezil, rivastigmine, etc.) and NMDA receptor antagonists (memantine), can only alleviate symptoms and cannot stop disease progression. In recent years, multi-target intervention strategies have become a research hotspot, but current technologies lack effective compositions that can simultaneously target multiple pathological processes such as mitochondrial dysfunction, oxidative stress, neuroinflammation, and Aβ deposition. In particular, how to improve the intervention effect while ensuring safety through the synergistic effect of specific ratios of natural active ingredients remains a technical problem that urgently needs to be solved in this field. In addition, although there are some nutritional supplement compositions for AD in the existing technology, they generally have the following problems:

[0005] 1. The formulation design lacks synergistic effects among the active ingredients;

[0006] 2. Key components such as curcumin and coenzyme Q10 have low bioavailability;

[0007] 3. There is a lack of effective technical means to improve the blood-brain barrier permeability of the composition;

[0008] 4. Its protective effect on neurons is limited, making it difficult to fully intervene in the various pathological processes of AD.

[0009] This invention utilizes magnetic fields and electromagnetic waves with specific parameters to act on matter, thereby altering its molecular arrangement and energy state. Through extensive experimentation, we have found that applying this technology to the post-processing stage of this pharmaceutical composition can significantly improve the bioavailability and therapeutic efficacy of the active ingredients.

[0010] This invention provides a pharmaceutical composition with synergistic effects, high bioavailability, and the ability to intervene in the pathological process of Alzheimer's disease (AD) at multiple targets, as well as a method for its preparation. Summary of the Invention

[0011] The purpose of this invention is to provide a pharmaceutical composition for the prevention and treatment of Alzheimer's disease and a method for its preparation. This invention achieves antioxidant, anti-inflammatory, cerebral blood flow improvement, and neuronal protection effects through the synergistic effect of multiple functional components.

[0012] The objective of this invention can be achieved through the following technical solutions:

[0013] A pharmaceutical composition for the prevention and adjunctive treatment of Alzheimer's disease comprises the following active ingredients in the indicated mass ratios: phosphatidylserine 100-200 mg, pyrrolquinone 10-20 mg, coenzyme Q10 50-200 mg, curcumin 50-200 mg, EGCG 50-200 mg, α-lipoic acid 100-300 mg, acetyl-L-carnitine 100-300 mg, magnesium threonate 50-100 mg, vitamin E 50-200 IU, folic acid 400-800 μg, and vitamin B12 10-50 μg; wherein the phosphatidylserine is pharmaceutical grade with a purity ≥90%, and the coenzyme Q10 and curcumin are nanoemulsified curcumin with a bioavailability ≥85%.

[0014] Furthermore, the pharmaceutical composition comprises the following active ingredients in the indicated weight ratios: phosphatidylserine 150 mg, pyrrolidone 15 mg, coenzyme Q10 125 mg, curcumin 125 mg, EGCG 125 mg, alpha-lipoic acid 200 mg, acetyl-L-carnitine 200 mg, magnesium threonate 75 mg, vitamin E 125 IU, folic acid 600 μg, and vitamin B12 30 μg.

[0015] Furthermore, the phosphatidylserine and EGCG are pharmaceutical grade with a purity of ≥90%.

[0016] Furthermore, the dosage form of the pharmaceutical composition is one of capsules, tablets, or powder.

[0017] A method for preparing a pharmaceutical composition for the prevention and adjunctive treatment of Alzheimer's disease, the method comprising the following steps: encapsulating a heat-sensitive component using microencapsulation technology to improve bioavailability.

[0018] Furthermore, the microencapsulation technology uses gum arabic, maltodextrin, β-cyclodextrin, chitosan oligosaccharide, or liposomes as wall materials, with a core-to-wall ratio of 1:(1-4).

[0019] Furthermore, the microencapsulation technology parameters are set as follows: inlet air temperature 160-180℃, outlet temperature 50-70℃, and atomization pressure 10-25MPa.

[0020] Furthermore, the preparation method also includes an energy loading step: placing the obtained composition powder in a weak magnetic resonance device for energy loading for 24-72 hours, with a frequency range of 1-20kHz and an intensity of 0.1-10mT.

[0021] Pyrroloquinoline quinone (PQQ) is a potent antioxidant that scavenge free radicals and reduce oxidative stress. Oxidative stress is closely related to the pathogenesis of Alzheimer's disease; therefore, the antioxidant properties of PQQ may help protect neurons from damage. Coenzyme Q10 (CoQ10) is a naturally occurring antioxidant in the human body, primarily functioning in the mitochondria of cells, participating in energy production and cellular metabolism. Both have antioxidant properties, but PQQ focuses more on promoting mitochondrial biosynthesis, while CoQ10 mainly participates in energy production. The combination of PQQ and CoQ10 has a synergistic effect: PQQ repairs damage to the mitochondrial network structure, while CoQ10 restores energy metabolic flow, synergistically inhibiting the neurotoxic cascade triggered by Aβ deposition.

[0022] Phosphatidylserine (PS) is an important phospholipid widely distributed in cell membranes, especially in the membrane structures of nerve cells. PS helps maintain the integrity of nerve cell membranes and promotes the transmission of nerve signals. Vitamin E is a fat-soluble antioxidant that plays a crucial role in protecting cell membranes from oxidative damage. The combined use of PS and vitamin E has a synergistic effect: PS maintains synaptic membrane integrity, providing a target for vitamin E, while vitamin E reduces oxidative stress damage, ensuring normal PS function and synergistically reducing Aβ-induced neuronal apoptosis.

[0023] Vitamin B12 and folic acid are two important water-soluble vitamins essential for the health and function of the nervous system. They interact in the body, jointly participating in homocysteine ​​metabolism, reducing neurotoxicity, promoting myelin repair and neurotransmitter synthesis, thereby synergistically improving cognitive function and slowing the progression of Alzheimer's disease. A deficiency in either can lead to elevated homocysteine ​​levels, thus increasing the risk of Alzheimer's disease.

[0024] Lipoic acid can enhance mitochondrial biosynthesis, and its powerful antioxidant properties can block oxidative stress-induced vascular endothelial damage, thereby improving cardiovascular health and reducing the risk of high-risk comorbidities of Alzheimer's disease such as hypertension and diabetes.

[0025] L-carnitine plays an important role in fatty acid metabolism, helping to transport fatty acids to mitochondria for energy production. Its regulation of acetyl-CoA pool stability can inhibit histone deacetylase activity and alleviate epigenetic abnormalities in Alzheimer's disease.

[0026] Curcumin and EGCG have shown potential in Alzheimer's disease research, possibly slowing disease progression through their antioxidant, anti-inflammatory, and amyloid protein aggregation-inhibiting effects. Specifically, curcumin reduces Aβ production stress, while epigallocatechin gallate enhances clearance efficiency, synergistically reducing Aβ plaque burden in the cortex. Furthermore, curcumin alleviates neuroinflammation by inhibiting the NF-κB pathway, while EGCG reduces tau protein hyperphosphorylation by regulating GSK-3β phosphorylation, thus doubly blocking core pathological links in neurodegenerative diseases.

[0027] Magnesium is an essential mineral for the human body, participating in various physiological functions such as energy metabolism, protein synthesis, nerve conduction, and muscle contraction. Magnesium L-threonate can cross the blood-brain barrier to reach the brain, directly increasing cerebrospinal fluid magnesium concentration, regulating the GSK-3β / tau phosphorylation balance, and inhibiting NLRP3 inflammasome activation.

[0028] In drug delivery systems, the synergistic effect of weak magnetic resonance and biomagnetic fields enhances efficacy through multi-level physical-biological coupling effects. Under the influence of quantum tunneling, a weak magnetic resonance field of a specific frequency resonates with the magnetic moment of drug molecules, significantly altering their Brownian motion mode and enhancing their directional diffusion capabilities, allowing the drug composition to overcome the limitations of passive diffusion. Simultaneously, the weak magnetic field modulates the conformation of cell membrane ion channels through Lorentz forces, inducing membrane potential fluctuations and forming a transient electroporation effect, promoting the transmembrane transport of macromolecular drugs. The mechanical waves generated by the magnetostrictive effect further activate the mitochondrial metabolic network, improving ATP synthesis efficiency and forming a positive feedback mechanism for drug redistribution. This multi-target magnetobiological intervention not only achieves triple optimization of cell membrane permeability, blood circulation, and cell metabolism, but also generates a synergistic effect through quantum magnetic targeting, ultimately improving drug delivery efficiency.

[0029] The beneficial effects of this invention are:

[0030] 1. Multi-target synergistic effect: The active ingredients of this invention work synergistically through different mechanisms, comprehensively intervening in multiple pathological processes of Alzheimer's disease (AD) through antioxidation, anti-inflammation, metabolic regulation, and neuroprotection. PQQ and coenzyme Q10 work together to repair mitochondrial function; phosphatidylserine and vitamin E work synergistically to protect neuronal cell membranes; B vitamins regulate homocysteine ​​metabolism; curcumin and EGCG work together to inhibit Aβ deposition and tau protein phosphorylation.

[0031] 2. High Bioavailability: This invention utilizes nanoemulsification and microencapsulation technologies to process key components, significantly improving their stability and bioavailability. After optimizing the molecular state of the composition using weak magnetic resonance imaging (fMRI), the solubility and blood-brain barrier permeability of the composition are further enhanced. This invention significantly improves drug delivery efficiency through weak magnetic resonance imaging; the quantum tunneling effect promotes the directional diffusion of drug molecules, overcoming the passive diffusion limit; Lorentz force regulation induces membrane potential fluctuations and electroporation effects, enhancing the transmembrane transport of macromolecules; magnetostrictive mechanical waves activate the mitochondrial metabolic network, forming a positive feedback loop for ATP synthesis. This triple optimization of cell membrane permeability, microcirculation, and metabolic activity significantly improves drug delivery efficiency.

[0032] 3. Advanced preparation process: Differentiated microencapsulation technology is used to process components with different properties to ensure the optimal activity of each component.

[0033] 4. High safety: All ingredients are naturally extracted or substances inherent in the human body. They are scientifically formulated and processed with advanced technology, resulting in minimal toxicity and side effects, making them suitable for long-term use. Attached Figure Description

[0034] To facilitate understanding by those skilled in the art, the present invention will be further described below with reference to the accompanying drawings.

[0035] Figure 1 A typical swimming trajectory of a mouse in a hidden platform task;

[0036] Figure 2 The time required for the mouse to escape from the water to the platform;

[0037] Figure 3 Representative photomicrographs (100 μm) of Congo red-stained aβ plaques in the hippocampus and somatosensory cortex of mice.

[0038] Figure 4 The proportion of Aβ plaques in the hippocampus region of the mouse brain;

[0039] Figure 5 The proportion of Aβ plaques in the mouse cerebral cortex. Detailed Implementation

[0040] To further illustrate the technical means and effects of the present invention in achieving its intended purpose, the following detailed description of the specific implementation methods, structures, features, and effects of the present invention, in conjunction with the accompanying drawings and preferred embodiments, is provided.

[0041] Example 1: The pharmaceutical composition comprises the following active ingredients in the indicated mass ratios: phosphatidylserine 200 mg, pyrroloquinoline quinone 15 mg, coenzyme Q10 125 mg, curcumin 125 mg, EGCG 125 mg, α-lipoic acid 200 mg, acetyl-L-carnitine 200 mg, magnesium threonate 75 mg, vitamin E 125 IU, folic acid 600 μg, and vitamin B12 30 μg;

[0042] A method for preparing a pharmaceutical composition for the prevention and treatment of Alzheimer's disease, the method comprising the following steps:

[0043] Phosphatidylserine, pyrroloquinoline quinone, coenzyme Q10, curcumin, EGCG and vitamin E were encapsulated using microencapsulation technology, with β-cyclodextrin as the wall material. The inlet air temperature was 170℃, the outlet temperature was 60℃, the atomization pressure was 15MPa, and the core-to-wall ratio was 1:2 to obtain a mixture.

[0044] The microencapsulated mixture and other components in the combination were thoroughly mixed and granulated, and then placed in a weak magnetic resonance device for energy loading for 48 hours at a frequency range of 10 kHz and an intensity of 5 mT to obtain the pharmaceutical composition for the prevention and treatment of Alzheimer's disease.

[0045] Example 2: Solubility Test

[0046] The mixture treated with microencapsulation technology in Example 1 and the untreated mixture were respectively added to simulated intestinal fluid (pH 6.8), shaken at 37°C to dissolve, and their solubility was measured.

[0047] Experimental materials:

[0048] 1. Preparation of simulated intestinal fluid (pH 6.8)

[0049] Ingredients: Potassium dihydrogen phosphate (KH2PO4, 0.05M); Sodium hydroxide (NaOH, to adjust pH); Pancreatic enzyme (10mg / mL).

[0050] Steps: Dissolve KH2PO4, adjust the pH to 6.8 with NaOH, and add trypsin.

[0051] Experimental methods:

[0052] 2. Simulated intestinal fluid test

[0053] Take 900 mL of simulated intestinal fluid into a dissolution vessel and preheat it to 37°C. Add the sample, start stirring (50 rpm, USPII method), take a sample, and analyze it.

[0054] Experimental results:

[0055] In simulated intestinal fluid, the solubility of the microencapsulated group reached 86.5%, while that of the untreated group was 9.1%.

[0056] Example 3: Experiment on the synergistic effect of pyrroloquinoline quinone (PQQ) and coenzyme Q10

[0057] Fifty Balb / c mice (weighing 20g-22g) were selected and acclimatized for one week, then randomly divided into 5 groups:

[0058] Group A: Blank control group (Control):

[0059] Group B: Basic feed + physiological saline (by gavage).

[0060] Group C: Basic feed + PQQ (1.5mg / kg / day, by gavage).

[0061] Group D: Basic feed + CoQ10 (30mg / kg / day, by gavage).

[0062] Group E: Basic feed + PQQ + CoQ10 (dosage same as the single group, administered by gavage).

[0063] After 4 weeks of continuous administration, the animals were sacrificed after fasting for 12 hours, and brain tissue homogenates were collected for analysis of ATP levels, MDA content, SOD / GSH-Px activity, and other indicators.

[0064] Experimental results:

[0065] The study found that, as nutrients for mitochondria, both PQQ and CoQ10 supplementation alone significantly increased ATP, and the combined group showed a further synergistic enhancement, improving energy metabolism. Furthermore, both PQQ and CoQ10 have strong antioxidant effects; supplementation alone reduced MDA, but the combined group showed a more significant effect, indicating that they synergistically alleviate lipid peroxidation damage in brain tissue. PQQ's activation effect on SOD was stronger than CoQ10, and the combined group showed a significantly higher effect than the individual groups, suggesting a synergistic effect of the antioxidant defense system. The results are shown in the table below:

[0066] Table 1 shows the effects of PQQ and CoQ10 on brain tissue energy metabolism and antioxidant levels.

[0067] Note: *vs. blank control group: *p<0.05, **p<0.01, ***p<0.001

[0068] *vs. Individual supplementation group (PQQ or CoQ10): p<0.05

[0069] Example 4: Animal experiment on the synergistic effect of phosphatidylserine (PS) and vitamin E

[0070] Fifty Balb / c mice (weighing 20g-22g) were selected and acclimatized for one week, then randomly divided into 5 groups:

[0071] Group A: Blank control group (Control):

[0072] Group B: Basic feed + physiological saline (by gavage).

[0073] Group C: Basic feed + PS (30mg / kg / day, by gavage).

[0074] Group D: Basic feed + Vitamin E (15mg / kg / day, by gavage).

[0075] Group E: Basic feed + PS + VE (dosage same as the single group, administered by gavage).

[0076] After 4 weeks of continuous administration, the animals were sacrificed after fasting for 12 hours, and brain tissue homogenates were collected for analysis of ATP levels, MDA content, SOD / GSH-Px activity, and other indicators.

[0077] Experimental results:

[0078] (1) Oxidative stress indicators (MDA, SOD, CAT, GSH-Px)

[0079] PS may enhance cell membrane stability, while VE directly scavenge free radicals. Both PS and VE supplementation alone significantly reduced MDA and increased the activity of antioxidant enzymes (SOD, CAT, GSH-Px), indicating that both can alleviate oxidative damage in brain tissue. Furthermore, the PS+VE combination group showed the strongest effect, suggesting a synergistic antioxidant effect.

[0080] (2) Acetylcholinesterase (AChE) activity

[0081] The study found that PS alone may improve cognitive function by protecting neuronal cell membranes and reducing acetylcholine degradation. VE alone had a smaller effect, but the PS+VE combination group showed more significant AChE inhibition, suggesting that PS plays a major role in regulating the cholinergic system, while VE may provide auxiliary protection. The results are shown in the figure below:

[0082] Table 1 Effects of PS and VE on Oxidative Stress and Cholinergic System in Brain Tissue

[0083] Note: *vs. blank control group p<0.05, **p<0.01, ***p<0.001

[0084] *vs Individual supplement group (PS or VE) p<0.05

[0085] Example 5: Animal experiment on the synergistic effect of curcumin and EGCG

[0086] Objective: To investigate the effects of curcumin and epigallocatechin gallate (EGCG), alone or in combination, on inflammatory factors (TNF-α, IL-6, IL-1β) and amyloid deposition (Congo red staining) in brain tissue. To explore the anti-inflammatory and anti-amyloid deposition effects of these two natural antioxidants and their potential synergistic effects.

[0087] Experimental methods: Fifty Balb / c mice (weighing 20g-22g) were selected and acclimatized for one week, then randomly divided into 5 groups:

[0088] Group A: Blank control group (Control):

[0089] Group B: Basic feed + physiological saline (by gavage).

[0090] Group C: Basic feed + curcumin (20mg / kg / day, by gavage).

[0091] Group D: Basic feed + EGCG (15mg / kg / day, by gavage).

[0092] Group E: Basic feed + curcumin + EGCG (dosage same as the single group, administered by gavage).

[0093] After 4 weeks of continuous administration, the animals were sacrificed after fasting for 12 hours, and brain tissue homogenates were collected for analysis of indicators such as TNF-α, IL-6, IL-1β, and β-amyloid (Aβ) deposition.

[0094] Experimental results:

[0095] (1) Anti-inflammatory effects (TNF-α, IL-6, IL-1β)

[0096] Studies have found that curcumin and EGCG, used alone, significantly reduce pro-inflammatory factors, with the combined group showing a stronger effect, suggesting a synergistic inhibition of neuroinflammation.

[0097] (2) Anti-amyloid deposition (Congo red staining)

[0098] The results showed that both components reduced Aβ deposition, and the combined intervention had the best effect.

[0099] Effects of curcumin and EGCG on brain tissue inflammation and amyloid deposition

[0100] Note: *vs. blank control group: *p<0.05, **p<0.01, ***p<0.001

[0101] *vs. group receiving supplementation alone (curcumin or EGCG): p<0.05

[0102] Example 6: Animal Experiment

[0103] Fifty 12-month-old APP / PS1 transgenic AD model mice were randomly divided into 5 groups:

[0104] Group A: Normal control group (wild-type mice);

[0105] Group B: AD model control group;

[0106] Group C: AD model + donepezil (positive control);

[0107] Group D: AD model + composition of Example 1 of this invention (without weak magnetic resonance treatment);

[0108] Group E: AD model + composition of Example 1 of the present invention (treated with weak magnetic resonance).

[0109] After 12 weeks of continuous administration, the following tests were performed:

[0110] 1. Morris water maze experiment: to measure spatial learning and memory abilities;

[0111] 2. Brain tissue was collected for Aβ immunohistochemical staining to quantitatively analyze the number of plaques;

[0112] result:

[0113] 1. Improvement in spatial memory in mice

[0114] APP / PS1 mice exhibit increased Aβ plaque formation and cognitive decline with age. For example... Figure 1 and Figure 2 As shown, compared with group A, group B exhibited impaired acquired spatial learning ability. In the continuous water maze experiment, the model group mice showed a slower reduction in escape latency. Group E, however, had a significantly shorter escape latency than the other groups. On days 8 and 9, the platform was removed, and the mice's spatial exploration and memory abilities were observed. The results showed that, compared with groups C and D, group E not only showed significant improvement in spatial learning but also a significant improvement in spatial memory ability (p<0.01 compared to the model group; p<0.05 compared to groups C and D).

[0115] 2. Changes in the number of β-amyloid (Aβ) plaques in the mouse brain

[0116] At 7 months, compared with the normal control group, the model group mice showed a significant increase in Aβ plaque deposition in the hippocampus and cortex. Treatment in group E significantly reduced Aβ plaque deposition in the hippocampus and cortex (P<0.01), and the effect was significantly stronger than that in groups C and D (P<0.05).

[0117] Example 7: Clinical efficacy verification

[0118] Sixty patients aged 60-75 years with mild cognitive impairment were randomly divided into an experimental group (the composition of Example 1 of this invention) and a control group (placebo), and observed in a double-blind manner for 6 months. The primary endpoint was the change in ADAS-cog score, and secondary endpoints included MMSE score, cerebrospinal fluid Aβ42 level, and Activities of Daily Living (ADL) scale.

[0119] Results: 1. ADAS-cog score: The experimental group showed an improvement of 2.5±1.2 points, while the control group showed a deterioration of 3.8±1.5 points (P<0.01).

[0120] 2. MMSE score: The experimental group improved by 1.8±0.9 points, while the control group decreased by 2.2±1.1 points (P<0.01).

[0121] 3. Cerebrospinal fluid Aβ42: The level increased by 15.6% in the experimental group and decreased by 8.3% in the control group (P<0.05).

[0122] 4. Incidence of adverse reactions: 6.7% in the experimental group and 5.0% in the control group (P>0.05)

[0123] As can be seen from the examples and comparative data, the pharmaceutical composition prepared in this invention has a positive effect on the cognitive function of patients with mild cognitive impairment and Alzheimer's disease.

[0124] The above description is merely a preferred embodiment of the present invention and is not intended to limit the present invention in any way. Although the present invention has been disclosed above with reference to preferred embodiments, it is not intended to limit the present invention. Any person skilled in the art can make some modifications or alterations to the above-disclosed technical content to create equivalent embodiments without departing from the scope of the present invention. Any simple modifications, equivalent changes and alterations made to the above embodiments based on the technical essence of the present invention without departing from the scope of the present invention shall still fall within the scope of the present invention.

Claims

1. A pharmaceutical composition for the prevention and adjunctive treatment of Alzheimer's disease, characterized in that, It is composed of the following active ingredients in the indicated mass ratios: phosphatidylserine 100-200 mg, pyrrolquinone 10-20 mg, coenzyme Q10 50-200 mg, curcumin 50-200 mg, EGCG 50-200 mg, α-lipoic acid 100-300 mg, acetyl-L-carnitine 100-300 mg, magnesium threonate 50-100 mg, vitamin E 50-200 IU, folic acid 400-800 μg, and vitamin B12 10-50 μg; wherein, the phosphatidylserine is pharmaceutical grade with a purity ≥90%, and the coenzyme Q10 and curcumin are nano-emulsified curcumin with a bioavailability ≥85%; The preparation method of the pharmaceutical composition includes the following steps: encapsulating the heat-sensitive component using microencapsulation technology to improve bioavailability and stability; The preparation method further includes an energy loading step: the prepared composition powder is placed in a weak magnetic resonance device for energy loading for 24-72 hours, with a frequency range of 0.1-20kHz and an intensity of 0.1-10mT.

2. The pharmaceutical composition for the prevention and adjunctive treatment of Alzheimer's disease according to claim 1, characterized in that, The pharmaceutical composition comprises the following active ingredients in the indicated weight ratios: phosphatidylserine 150 mg, pyrrolidone 15 mg, coenzyme Q10 125 mg, curcumin 125 mg, EGCG 125 mg, alpha-lipoic acid 200 mg, acetyl-L-carnitine 200 mg, magnesium threonate 75 mg, vitamin E 125 IU, folic acid 600 μg, and vitamin B12 30 μg.

3. The pharmaceutical composition for the prevention and adjunctive treatment of Alzheimer's disease according to claim 1, characterized in that, The phosphatidylserine and EGCG are pharmaceutical grade with a purity of ≥90%.

4. A pharmaceutical composition for the prevention and adjunctive treatment of Alzheimer's disease according to claim 1, characterized in that, The dosage form of the pharmaceutical composition is one of capsules, tablets, or powder.

5. A pharmaceutical composition for the prevention and adjunctive treatment of Alzheimer's disease according to claim 1, characterized in that, The microencapsulation technology uses gum arabic, maltodextrin, β-cyclodextrin, chitosan oligosaccharide or liposomes as wall materials, with a core-to-wall ratio of 1:(1-4).

6. A pharmaceutical composition for the prevention and adjunctive treatment of Alzheimer's disease according to claim 1, characterized in that, The microencapsulation technology parameters are set as follows: inlet air temperature 160-180℃, outlet temperature 50-70℃, and atomization pressure 10-25MPa.

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