KR100787765B1 - Composition comprising palmitic acid for preventing or treating alzheimer's disease - Google Patents

Abstract

A composition comprising palmitic acid is provided to inhibit the oxidative stress induced by amyloid beta peptide excellently and secure excellent cell survival rate, thereby being usefully used for preventing or treating Alzheimer's disease. A pharmaceutical composition for preventing or treating Alzheimer's disease comprises palmitic acid which is obtained by extracting Gardenia jasminoides with water, alcohol or a mixture of water and alcohol, filtering the extract, concentrating the filtrate under reduced pressure and then freeze-drying the concentrate. A food composition useful for preventing Alzheimer's disease comprises palmitic acid extracted and isolated from Gardenia jasminoides.

Description

Composition comprising palmitic acid for preventing or treating Alzheimer's disease

1 is a diagram showing the inhibitory activity of oxidative stress induced by hydrogen peroxide in PC12 cells of Gardenia ethanol extract according to the present invention.

(C: group not treated with hydrogen peroxide (H ₂ O ₂ ),

 H: group treated with 100 μM hydrogen peroxide,

 V: group treated with 100 μM Vit C for 48 hours before treatment with hydrogen peroxide,

 G: group treated with 0.1 mg / ml of Gardenia ethanol extract for 48 hours before treatment with hydrogen peroxide)

Figure 2 is a diagram showing the inhibitory activity of oxidative stress induced by amyloid beta peptides in PC12 cells of the gardenia fraction according to the present invention.

(C: group not treated with amyloid beta peptide (Aβ _25-35 ),

A: group treated with 10 μM amyloid beta peptide (Aβ _25-35 ),

V: group treated with 100 μM Vit C for 48 hours prior to treatment with amyloid beta peptide (Aβ _25-35 ),

H1 ~ E3: Gardenia hexane fraction (H1 ~ H3), gardenia chloroform fraction (C1 ~ C3) and gardenia ethyl acetate fraction (E1 ~ E3) for 20 hours before treatment with amyloid beta peptide (Aβ _25-35 ). Group treated with μl (1 mg / ml))

Figure 3 is an analysis of HPLC of palmitic acid, the active substance isolated from the gardenia ethyl acetate fraction according to the present invention.

The present invention relates to a composition for preventing or treating Alzheimer's disease comprising palmitic acid.

Alzheimer's disease (AD) is a degenerative neurological disease, affecting about 50% of people aged 80 and older. Alzheimer's disease is the fourth leading cause of death in the elderly, after cancer, heart disease and stroke. In the United States, more than 250,000 people are diagnosed with Alzheimer's disease every year, and it is estimated that 4 million patients currently have it. .

Alzheimer's disease is largely classified into hereditary Alzheimer's disease (FAD) and sporadic Alzheimer's disease (SAD).

Hereditary Alzheimer's disease accounts for 5-10% of all Alzheimer's disease patients, including presenilin 1 (PS1), amyloid precursor protein (APP), and presenilin 2 (known as causative genes). Presenilin 2 (PS2) mutations cause 100% Alzheimer's disease.

Sporadic Alzheimer's disease accounts for the majority of Alzheimer's disease patients and is more likely to develop Alzheimer's disease when mutations occur in apolipoprotein E (ApoE) or alpha-2 macroglobulin (A2M). Risk factors are known, but the exact cause of the disease is unknown.

Pathological characteristics of Alzheimer's disease include senile plaques that accumulate outside the neurons, neurofibrilary tangles that appear to be tangled in the cell bodies of neurons, and neuronal loss. Etc. can be mentioned. This pathological feature is present in all cases of hereditary Alzheimer's disease and sporadic Alzheimer's disease, among which toxic protein called amyloid β peptide (Aβ) has been identified as a major component of senile plaques. Amyloid beta peptides are insoluble peptides consisting of 40 to 42 amino acids resulting from abnormal cleavage of amyloid proproteins. It is also reported that overaccumulation of amyloid beta peptides is a common phenomenon in all cases of hereditary Alzheimer's disease and sporadic Alzheimer's disease. Amyloid beta peptides are therefore considered to be the major pathogenic material of Alzheimer's disease.

The overall pathogenesis of Alzheimer's disease is as follows. Mutations in the presenilin 1 and 2 genes (PS 1 and 2) result in abnormal cleavage of amyloid proproteins and production of amyloid beta peptides by beta-secretase. The resulting amyloid beta peptide causes necrosis of neuronal cells, which causes Alzheimer's disease.

As indicated above, inactivation and necrosis of the cranial nerve is thought to be cytotoxic by amyloid beta peptide, an abnormal metabolite of amyloid proprotein. Its neurotoxicity begins with brain nerve cell destruction caused by oxidative stress. The cause of neural cell necrosis in Alzheimer's disease is still unclear, but the production of oxygen free radicals and oxidative injury such as reactive oxygen species (ROS) can lead to neuronal cell destruction and pathogenesis. It is assumed to be related to).

Currently, an increase in these oxidative stresses (reactive oxygen species (ROS), lipid peroxidation, protein modification, mitochondrial DNA oxidation) in the brains of Alzheimer's disease patients is demonstrated. In addition, since amyloid beta peptides induce intracellular free radical status and ultimately induce apoptosis, cell breakdown is thought to be correlated with amyloid beta peptides.

Recently, research on Alzheimer's disease has been focused on brain cell destruction by amyloid beta peptides, the structure and physiology of these proteins, and the decrease of acetylcholine (ACh) due to accumulation in the brain.

Symptoms of Alzheimer's disease include a slow progression of memory, cognition, and learning, which can lead to emotional disorders and abnormal behavior. Therefore, the treatment of Alzheimer's disease has been the only treatment, indirect treatment mainly focused on lightening the patient's symptoms and slowing the progression of the disease.

The dementia treatments reported to date are drugs that improve cognitive symptoms in patients with senile dementia. Inhibitors of acetylcholinesterase, which are closely related to the concentration of neurotransmitter called acetylcholine in the brain hippocampus (acetylcholine esterase inhibitor) is used a lot.

Acetylcholinesterase is an acetylcholine having a quaternary amine structure and is a neurotransmitter, and acts as a choline by hydrolyzing acetylcholine. In patients with dementia, the concentration of acetylcholine, a neurotransmitter, is reduced, and when acetylcholinesterase is inhibited, the concentration of acetylcholine in the brain is increased to improve symptoms of dementia patients. Drugs that are currently being developed and used in the treatment of dementia with FDA approval include tacrine, donepezil, rivastigmine and metrifonate.

The first generation of acetylcholinesterase inhibitors are tacrine, the first drug to be approved for antidementia. However, due to the short duration of action of tacrine, it should be administered 4 times a day.

Second-generation acetylcholinesterase inhibitors are developed by Ezaisa, Japan, approved by the US FDA at the end of 1996, and sold in 30 countries around the world since 1997. These drugs can be taken once a day. And selective inhibition has the effect of reducing peripheral side effects.

Rivastigmine is a drug developed by Novartis in the United States, approved in December 1997 in Switzerland, and used in the European Union (EU) and South American countries, and in preparation for approval in the United States and Canada, and introduced in September 1997 in Korea. It became. The drug can be taken twice a day and is highly specific to the central nervous system, greatly reducing peripheral side effects, and reported to have little liver toxicity due to metabolism in the kidneys.

Metrifonate is undergoing a phase 3 clinical trial in patients with dementia and has a long duration of action as an irreversible acetylcholinesterase inhibitor.

As mentioned above, currently used dementia therapeutic agents are mostly acetylcholinesterase inhibitors.

On the other hand, since amyloid beta peptides are thought to be at least one cause of Alzheimer's disease, the development of a substance that inhibits damage to brain neurons caused by oxidative stress induced by amyloid beta peptides is effective in preventing or treating Alzheimer's disease. I think it will be.

Therefore, studies on genetic approaches to inhibit or block amyloid beta peptide generation and cytotoxicity induced by amyloid beta peptides have been relatively active in domestic researchers. However, the development of drugs as a prophylactic or therapeutic agent for Alzheimer's disease using the same is still insufficient.

Accordingly, the inventors of the present invention, while searching for a substance in the herbal medicine that can inhibit damage to the brain neurons caused by oxidative stress induced by amyloid beta peptides, palmitic acid amyloid beta peptide is an active substance extracted and separated from gardenia The present invention has been found to significantly reduce the oxidative stress induced by.

The present invention is to provide a composition for the prevention or treatment of Alzheimer's disease comprising palmitic acid.

The present invention provides a composition for the prevention or treatment of Alzheimer's disease comprising palmitic acid.

Compositions according to the present invention include pharmaceutical compositions and food compositions.

Hereinafter, the present invention will be described in detail.

Palmitic acid, which is an active ingredient in the composition of the present invention, was extracted and separated from Gardenia jasminoides, and extracted and separated from other herbal medicines, prepared by a chemical synthesis method, or a commercially available reagent can be purchased and used.

Palmitic acid according to the present invention is Gardenia jasminoides ) is added to water, alcohol or a mixed solvent of water and alcohol, shaken and extracted at room temperature for 24 hours (repeat 5 times). The extract was filtered, concentrated under reduced pressure, and lyophilized to obtain a gardenia extract. The mixed solvent of water and alcohol may be selected from 10 to 100% methanol or 10 to 100% ethanol, preferably 10 to 100% ethanol.

Water was added to the gardenia extracts and suspended uniformly, and then hexane was added thereto to extract reflux (3 times). Chloroform was added to the obtained water layer and refluxed (3 times). Ethyl acetate was added to the obtained water layer and refluxed (3 times). The amount of the extraction solvent hexane, chloroform and ethyl acetate is used in an amount corresponding to three times the volume (ml) of the Gardenia alcohol extract (g). The solvent of each gardenia fraction obtained by extraction as described above was removed and lyophilized to obtain the gardenia hexane fraction, the gardenia chloroform fraction and the gardenia ethyl acetate fraction, respectively.

Silica gel column chromatography using a mixed solvent of chloroform: ethanol (100-0: 0-100) as the mobile phase solvent of the gardenia ethyl acetate fraction having the highest inhibitory activity against oxidative stress induced by amyloid beta peptide among the gardenia fractions Open column chromatography is performed to fractionate 29 gardenia subfractions. Among them, the second fraction of 40:60 chloroform: ethanol having the highest inhibitory activity against oxidative stress induced by amyloid beta peptides is obtained through HPLC analysis to obtain an active substance palmitic acid.

Palmitic acid according to the present invention has excellent inhibitory activity and cell survival rate of oxidative stress induced by amyloid beta peptides, and thus can be used as medicines and health foods useful for the prevention or treatment of Alzheimer's disease.

The composition of the present invention may contain one or more known active ingredients having a prophylactic or therapeutic effect with Alzheimer's disease together with palmitic acid.

The composition of the present invention may be prepared by including one or more pharmaceutically acceptable carriers in addition to the above-described active ingredients for administration. Pharmaceutically acceptable carriers may be used in combination with saline, sterile water, Ringer's solution, buffered saline, dextrose solution, maltodextrin solution, glycerol, ethanol and one or more of these components, Other conventional additives such as buffers and bacteriostatic agents can be added. Diluents, dispersants, surfactants, binders and lubricants may also be added in addition to formulate into injectable formulations, pills, capsules, granules or tablets such as aqueous solutions, suspensions, emulsions and the like. Furthermore, it may be preferably formulated according to each disease or component by a suitable method in the art or using a method disclosed in Remington's Pharmaceutical Science (Recent Edition), Mack Publishing Company, Easton PA.

The composition of the present invention can be administered orally or parenterally (eg, applied intravenously, subcutaneously, intraperitoneally or topically) according to the desired method, and the dosage is based on the weight, age, sex and health of the patient. The range varies depending on the diet, the time of administration, the method of administration, the rate of excretion and the severity of the disease. The daily dose of palmitic acid is about 1 to 30 mg / kg, preferably about 4 to 12 mg / kg, and more preferably administered once to several times a day.

The composition of the present invention can be used alone or in combination with methods using surgery, hormone therapy, drug therapy and biological response modifiers for the prevention or treatment of Alzheimer's disease.

The composition of the present invention can be added to health food for the purpose of improving Alzheimer's disease. When palmitic acid of the present invention is used as a food additive, the palmitic acid may be added as it is or used with other foods or food ingredients, and may be appropriately used according to a conventional method. The mixed amount of the active ingredient may be suitably determined depending on the purpose of use (prevention, health or therapeutic treatment). In general, in the preparation of food or beverage, palmitic acid of the present invention is added in an amount of 15% by weight or less, preferably 10% by weight or less based on the raw material. However, in the case of long-term intake for health and hygiene or health control, the amount may be below the above range, and the active ingredient may be used in an amount above the above range because there is no problem in terms of safety. .

There is no particular limitation on the kind of food. Examples of the food to which the substance can be added include dairy products including meat, sausage, bread, chocolate, candy, snacks, confectionery, pizza, ramen, other noodles, gums, ice cream, various soups, drinks, tea, drinks, Alcoholic beverages and vitamin complexes, and the like and include all of the health foods in the conventional sense.

The health beverage composition of the present invention may contain various flavors or natural carbohydrates, etc. as additional components, as in the general beverage. The above-mentioned natural carbohydrates are glucose, monosaccharides such as fructose, disaccharides such as maltose and sucrose, and polysaccharides such as dextrin and cyclodextrin, sugar alcohols such as xylitol, sorbitol and erythritol. As the sweetening agent, natural sweetening agents such as tautin and stevia extract, synthetic sweetening agents such as saccharin and aspartame, and the like can be used. The ratio of the natural carbohydrate is generally about 0.01 to 0.04 g, preferably about 0.02 to 0.03 g per 100 ml of the composition of the present invention.

In addition to the above, the composition of the present invention includes various nutrients, vitamins, electrolytes, flavoring agents, coloring agents, pectic acid and salts thereof, alginic acid and salts thereof, organic acids, protective colloid thickeners, pH adjusting agents, stabilizers, preservatives, glycerin, alcohols, carbonic acid. Carbonating agents and the like used in beverages. In addition, the composition of the present invention may contain a pulp for the production of natural fruit juices, fruit juice drinks and vegetable drinks. These components can be used independently or in combination. The proportion of such additives is not critical but is generally selected in the range of 0.01 to 0.1 parts by weight per 100 parts by weight of the composition of the present invention.

Hereinafter, preferred examples are provided to aid in understanding the present invention. However, the following examples are merely provided to more easily understand the present invention, and the contents of the present invention are not limited by the examples.

Example  One  : Separation of active substance from gardenia

1. Preparation of Gardenia Ethanol Extract

Gardenia ( Gardenia jasminoides ) were washed, dried and ground finely with a hand mixer. The ground gardenia (2.1 kg) was added to 10 L of ethanol and shaken for 24 hours at room temperature and extracted (5 times). The extract was filtered through a filter paper, concentrated under reduced pressure to remove the solvent, and freeze-dried to obtain a gardenia ethanol extract (600 g).

2. Gardenia Fraction  Produce

To the gardenia ethanol extract (600 g) obtained in 1, 200 ml of water was added and suspended uniformly, and thereafter, 600 ml of hexane was added thereto, followed by reflux extraction (3 times). 600 mL of chloroform was added to the obtained water layer, and the mixture was extracted under reflux (3 times). 600 mL of ethyl acetate was added to the obtained water layer, and the mixture was extracted under reflux (3 times). The solvent of each gardenia fraction obtained by extraction as described above was removed and lyophilized to obtain a gardenia hexane fraction, gardenia chloroform fraction and gardenia ethyl acetate fraction, respectively. Gardenia ethyl acetate fraction was obtained at about 4.88 g.

As a result of measuring the inhibitory activity of oxidative stress induced by amyloid beta peptide of each gardenia fraction according to Experimental Example 1, the inhibitory activity was the best in the gardenia ethyl acetate fraction.

3. Gardenia ethyl acetate From fractions  Isolation of Active Material

Silica gel column chromatography (open column) using a mixed solvent of chloroform: ethanol (100-0: 0-100) as the mobile phase solvent of the gardenia ethyl acetate fraction having the highest inhibitory activity against oxidative stress induced by amyloid beta peptides chromatography) was fractionated into 29 gardenia small fractions.

Among the 29 gardenia subfractions, the ratio of chloroform: ethanol was the best at inhibiting oxidative stress induced by amyloid beta peptide in the second fraction of 40:60.

In order to isolate the active substance in the fraction, HPLC analysis was performed under the following conditions. The isolated active material was identified as palmitic acid having a molecular weight of 256 m / z.

<HPLC analysis conditions>

Data detection: PDA, 240 nm

Peak: 6.7 min,

Column: μ-bondapak ^TM C ₁₈ reverse column (3.9 × 300 mm),

Mobile phase: gradient elution of 0-100% ethanol (53 minutes in total),

Speed: 0.5 ml / min,

Injection volume: 10 μl (10 mg / ml concentration).

Experimental Example  One  Gardenia Fraction  And amyloid beta peptides of the active substance isolated therefrom. Oxidative  Measurement of Inhibitory Activity of Stress

In order to investigate the inhibitory activity of oxidative stress induced by amyloid beta peptides of the gardenia fraction and the active substance isolated therefrom, the following experiment was carried out.

PC12 cells (brown cells, ATCC), the nervous system cell used in the experiment, were cultured in RPMI-1640 medium containing antimicotics / antibiotics.

1. Gardenia ethanol extract Oxidative  Inhibitory Activity of Stress

When the cell number of the cultured PC12 cells was 10 ⁴ ~ 10 ⁶ cells / ㎖ pre-incubated with 0.1 mg / ㎖ of the gardenia ethanol extract prepared in Example 1. After 48 hours, 10 μM of hydrogen peroxide (H ₂ O ₂ ) was treated to induce oxidative stress. In oxidative damage induced by hydrogen peroxide, the degree of oxidative stress produced using DCF-DA (2 ', 7'-dichlorofluoresine diacetate) was measured with a spectrofluorometer.

100 μM of Vit C was used as a positive control.

The results are shown in FIG.

As shown in Figure 1, it was confirmed that the oxidative stress induced by hydrogen peroxide in PC12 cells treated with Gardenia ethanol extract of the present invention is reduced.

2. Gardenia Fraction  And the active substance separated therefrom Oxidative  Inhibitory Activity of Stress

When the cell number of the cultured PC12 cells was 10 ⁴ to 10 ⁶ cells / ml, 20 μl (1 mg / g) of the gardenia hexane fraction, the gardenia chloroform fraction, the gardenia ethyl acetate fraction, and palmitic acid, respectively, isolated in Example 1 were obtained. Ml). After 48 hours, 10 μM of amyloid beta peptides (Aβ _25-35 ) were treated to induce oxidative stress. The oxidative damage induced by Aβ _25-35 was measured spectrophotometrically by the degree of oxidative stress produced using DCF-DA (2 ', 7'-dichlorofluoresine diacetate).

100 μM of Vit C was used as a positive control.

The results of the oxidative stress inhibitory activity of the gardenia fractions are shown in Figure 2, and the results of the oxidative stress inhibitory activity of palmitic acid are shown in Table 1.

※ C: group not treated with amyloid beta peptide (Aβ _25-35 ),

A: group treated with 10 μM amyloid beta peptide (Aβ _25-35 ),

V: group treated with 100 μM Vit C for 48 hours prior to treatment with amyloid beta peptide (Aβ _25-35 ),

* P <0.01 vs group (C) not treated with amyloid beta peptides (Aβ _25-35 ),

Group (A) treated with #P <0.01 versus amyloid beta peptide (Aβ _25-35 ).

As shown in Figure 2, it was confirmed that the oxidative stress induced by amyloid beta peptide (Aβ _25-35 ) in PC12 cells treated with the gardenia ethyl acetate fraction of the present invention was significantly reduced.

In addition, as shown in Table 1, the inhibitory activity of oxidative stress induced by amyloid beta-peptide in the second fraction of chloroform: ethanol ratio of 40:60 among 29 gardenia subfractions isolated from the gardenia ethyl acetate fraction was the most. Appeared excellent.

Experimental Example  2  Gardenia From fractions  Cell viability measurement of isolated active substance MTT  reduction assay )

In order to confirm the cell viability of the small gardenia fraction containing the active material according to the present invention, the following experiment was performed using the MTT reduction assay.

The number of cells of the cultured PC12 cells 10 ⁴ and 10 ⁶ treated with Example 20 ㎕ 1 a 29 gardenia small fraction prepared from each (1 ㎎ / ㎖) when the cell / ㎖, and after 48 hours 10 μM The amyloid beta peptide (Aβ _25-35 ) was treated to induce oxidative stress. After 24 hours, MTT [3- (4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide] reagent was added to observe the reaction. If PC12 cells survive the toxicity of Aβ _25-35 , mitochondrial respiration occurs and they react with NADH or NADPH produced by respiration to form purple formazan. The formed formazan was measured using a microplate reader (wavelength: observation 570 nm, reference value 630 nm).

The results are shown in Table 2.

※ C: group not treated with amyloid beta peptide (Aβ _25-35 ),

A: group treated with 10 μM amyloid beta peptide (Aβ _25-35 ),

V: group treated with 100 μM Vit C for 48 hours prior to treatment with amyloid beta peptide (Aβ _25-35 ),

* P <0.01 vs group (C) not treated with amyloid beta peptides (Aβ _25-35 ),

Group (A) treated with #P <0.01 versus amyloid beta peptide (Aβ _25-35 ).

As shown in Table 2, the ratio of chloroform: ethanol among the 29 gardenia subfractions isolated from the gardenia ethyl acetate fraction of the present invention showed the best cell viability in the second fraction of 40:60.

Therefore, palmitic acid extracted and isolated from the gardenia jasminoides according to the present invention can be seen that the most inhibited activity and cell survival rate of oxidative stress induced by amyloid beta peptide.

Examples of preparations for the compositions of the present invention are illustrated below.

Formulation example  One  : Preparation of Pharmaceutical Formulations

1. Preparation of powder

Palmitic acid 2 g

1 g lactose

The above ingredients were mixed and filled in airtight cloth to prepare a powder.

2. Preparation of Tablets

Palmitic acid 100 mg

Corn starch 100 mg

Lactose 100 mg

2 mg magnesium stearate

After mixing the above components, tablets were prepared by tableting according to a conventional method for producing tablets.

3. Preparation of Capsule

Palmitic acid 100 mg

Corn starch 100 mg

Lactose 100 mg

2 mg magnesium stearate

After mixing the above components, the capsule was prepared by filling in gelatin capsules according to the conventional method for producing a capsule.

Formulation example  2  : Manufacture of food

Food products containing palmitic acid of the present invention were prepared as follows.

1. Preparation of Cooking Seasonings

20 to 95% by weight of palmitic acid was prepared for cooking spices for health promotion.

2. Preparation of Tomato Ketchup and Sauce

Health-promoting tomato ketchup or sauce was prepared by adding 0.2-1.0 wt% palmitic acid to tomato ketchup or sauce.

3. Manufacturing of Flour Foods

0.5 to 5.0% by weight of palmitic acid was added to the flour, and the mixture was used to prepare bread, cake, cookies, crackers, and noodles to prepare health promoting foods.

4. Preparation of soups and gravy

0.1 to 5.0% by weight of palmitic acid was added to soups and broths to prepare meat products for health promotion, soups of noodles and broths.

5. Preparation of Ground Beef

10% by weight of palmitic acid was added to the ground beef to prepare a ground beef for health promotion.

6. Manufacture of Dairy Products

Palmitic acid 5-10% by weight was added to the milk, using the milk to prepare a variety of dairy products such as butter and ice cream.

Formulation example  3  : Preparation of Beverages

1. Preparation of carbonated drinks

5-10% of sugar, 0.05-0.3% citric acid, 0.005-0.02% caramel, 0.1-1% of vitamin C are mixed, and 79-94% purified water is mixed to make syrup, and the syrup is 85-98 Sterilizing at 20 ℃ for 180 seconds, mixed with cooling water in a ratio of 1: 4, and then injected with 0.5 to 0.82% of carbon dioxide gas to prepare a carbonated beverage containing palmitic acid of the present invention.

2. Manufacture of health drinks

Instant sterilization by homogeneous mixing of subsidiary materials such as liquid fructose (0.5%), oligosaccharide (2%), sugar (2%), salt (0.5%), water (75%) and palmitic acid , Packed in a small packaging container such as plastic bottles to prepare a healthy beverage.

3. Preparation of Vegetable Juice

5 g of palmitic acid was added to 1,000 ml of tomato or carrot juice to prepare vegetable juice for health promotion.

4. Preparation of Fruit Juice

1 g of palmitic acid was added to 1,000 ml of apple or grape juice to prepare a fruit juice for health promotion.

Palmitic acid according to the present invention has excellent inhibitory activity and cell survival rate of oxidative stress induced by amyloid beta peptides, and thus can be usefully used for the prevention or treatment of Alzheimer's disease.

Claims (4)

A pharmaceutical composition for preventing or treating Alzheimer's disease, including palmitic acid. The method of claim 1, wherein the palmitic acid is Gardenia jasminoides ) pharmaceutical composition for the prevention or treatment of Alzheimer's disease, characterized in that extracted and separated. A food composition useful for the prevention of Alzheimer's disease, including palmitic acid. The food composition of claim 3, wherein the palmitic acid is extracted and separated from the gardenia.

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