KR20210143707A - A composition comprising the Leaves of Schisandra chinensis for preventing or treating Parkinson's disease or neurodegenerative disease - Google Patents

Abstract

The present invention relates to a pharmaceutical composition and a health functional food for the prevention or treatment of stroke, Parkinson's disease and/or neurodegenerative disease, including Schisandra chinensis leaves. An extract of Schisandra chinensis leaves of the present invention reduces neuroinflammation, inhibits microglia activity, and has excellent effects of protecting brain neurons, thereby being able to be usefully used as a pharmaceutical composition or health functional food for preventing or treating stroke, Parkinson's disease and/or neurodegenerative disease.

Description

A composition for preventing or treating Parkinson's disease or neurodegenerative disease, comprising an extract of Schisandra leaf extract;

The present invention relates to a pharmaceutical composition and a health functional food for preventing or treating stroke, Parkinson's disease and/or neurodegenerative disease.

In 2000, the proportion of the population aged 65 and over in the total population reached 7.2%, and Korea entered an aging society. As such, as the aging problem has recently emerged as a social issue, the public's interest in the characteristics of the elderly population and the welfare of the elderly such as housing, health, culture, and leisure is increasing, and the demand for statistics is also increasing. The core of this change is that chronic degenerative diseases are emerging as a bigger problem than acute infectious diseases that have been the main cause of death for the past 50 years due to the increase in the aging population. In particular, among chronic degenerative diseases, death due to cerebrovascular disease is a very important disease that ranks second among deaths due to a single disease. For the prevention and treatment of these diseases, in Korea, a number of natural substances are marketed as health foods that are effective in the prevention of degenerative neurological diseases including stroke, but most of them have not undergone scientific verification, and are rather healthy. It is also a cause of food abuse and has become a social problem.

Neurodegenerative disease is a disease in which degenerative changes appear in nerve cells of the central nervous system, causing various symptoms such as impairment of motor and sensory functions, and inhibition of higher-order functions such as memory, learning, and computational reasoning. Representative diseases include Parkinson's disease, Alzheimer's disease, and memory impairment. Neurodegenerative diseases are characterized by rapid or slow progression of necrosis or death of nerve cells by apoptosis. Therefore, an understanding of the mechanism of neuronal cell death must be achieved for the prevention, control and development of treatments for central nervous system diseases.

The central nervous system consists of nerve cells and glial cells. Glia cells are the most distributed cells in the brain, accounting for 90% of the total brain cells and 50% of the total brain volume. Although these cells do not generate nerve impulses by themselves, they help neurons to perform their own functions, and are known to play a very important function in restoring brain tissue when it is damaged. The glial cells are again composed of three types of astrocytes, microglia, and oligodendroc ytes.

Among them, microglia (microglia), also called microglia, or microglia, are immune cells residing in the central nervous system (CNS) and occupy 5-10% of the total brain cells.

The microglia function as the first line of defense in the central nervous system. Microglia are a major endocellular source of inflammatory mediators in the central nervous system. Microglia are involved in neuroinflammation by producing nitric oxide (NO), reactive oxygen species (ROS), pro-inflammatory cytokines and prostaglandins. Activated microglia migrate to the damaged nervous tissue area to engulf and destroy microorganisms and cell debris.

However, the role of microglia as inflammatory cells is not always beneficial. Uncontrolled activation of microglia and persistent excessive neuroinflammation are thought to be the cause of various central nervous system pathologies including neurodegenerative diseases. That is, functionally activated microglia are known to cause neuronal cell death by producing and secreting inflammatory mediators.

Therefore, activation of microglia is related to various kinds of neurodegenerative diseases. For example, it is very well known that microglia play an important role in the formation of senile plague, even in Alzheimer's disease. An important example is that anti-inflammatory drugs, such as ibuprofen, can inhibit the formation of Noyophilus spots and prevent the onset of dementia.

On the other hand, Schisandra chinensis is a fruit of the Schisandra chinensis tree with a diameter of about 1 cm and a dark red color. It is used as a tonic by raising it. It is said to be helpful in treating cough and thirst as it strengthens lung function and has antitussive and expectorant effects. In addition, it is known that dried fruits are soaked in cold water, and honey and sugar are added to the boiled water to drink as a beverage, or to make hwachae or starch pyeon.

However, only research on medicinal efficacy and efficacy related to Schisandra fruit is being conducted, and research and development on other medicinal parts such as Schisandra leaf and Schisandra stem have never been made. In particular, it is necessary to conduct research and development on extracts from other parts of Schisandra, considering that the physiologically active substances of the fruit and leaves or stems are very different, and that Schisandra is generally used only as a fruit.

Under this background, the present inventors have completed the present invention by conducting research and development on a natural extract effective for degenerative neurological disease.

Korean Patent Application No. 10-2004-0067771

It is an object of the present invention to provide a pharmaceutical composition for the prevention or treatment of stroke or neurodegenerative disease, comprising the leaf extract of Schisandra leaf extract as an active ingredient.

In addition, it is an object of the present invention to provide a health functional food for preventing or improving stroke or neurodegenerative disease, comprising the Schisandra leaf extract as an active ingredient.

The present inventors completed the present invention by confirming that Schisandra leaf extract reduces neuroinflammation, inhibits microglia activity, and protects brain neurons while researching the effects of leaf extracts of Schisandra leaf extract.

The present invention relates to a pharmaceutical composition for preventing and treating stroke or neurodegenerative disease, comprising a leaf extract of Schisandra chinensis as an active ingredient.

Schisandra leaf extract of the present invention has a remarkable effect on the recovery of nerve damage caused by neuroinflammation and has an excellent effect on protecting cranial nerve cells, so it can be usefully used as a pharmaceutical composition for preventing or treating stroke or neurodegenerative disease. In particular, Schisandra leaf extract has a remarkable effect in the prevention and treatment of neurodegenerative diseases compared to other parts such as Schisandra fruit, and it is economically also has high efficacy.

The Schisandra leaf extract may be an extract extracted using water, alcohol, or a mixed solvent thereof as an extraction solvent, and the alcohol may preferably be a C ₁ to C ₄ lower alcohol. Preferably, the Schisandra leaf extract of the present invention is a Schisandra leaf hot water extract.

The neurodegenerative diseases include stroke, dementia, Alzheimer's disease, Parkinson's disease, Huntington's disease (chorea), Pick disease, Creutzfeld disease. -Jacob disease, frontotemporal dementia, dementia with Lewy bodies, amyotrophic lateral sclerosis (Lou Gehrig's disease), corticobasal degeneration, multiple systemic atrophy system atrophy), progressive supranuclear palsy, autoimmune disease, inflammatory and neuropathic pain, any one selected from the group consisting of neurovascular disease can be Preferably, the neurodegenerative disease may be Parkinson's disease.

In the preparation of the Schisandra leaf extract, extraction may be performed by shaking extraction, Soxhlet extraction, or reflux extraction, but is not limited thereto. The extraction temperature is preferably 40 to 100 ℃. In addition, the extraction time is preferably 0.5 to 24 hours, and the number of times of extraction is preferably 1 to 5 times.

As the extraction solvent used in the extraction, water, alcohol, or a mixture thereof may be used. It is preferable to use a lower alcohol of C ₁ to C _{4 as} the alcohol, and methanol or ethanol may be used. The extraction solvent according to the present invention is most preferably water extraction. In addition, it is preferable to extract by adding an extraction solvent 5 to 15 times the weight or volume of the prepared Schisandra leaf, and it is more preferable to extract by adding 10 times.

The extract may be concentrated under reduced pressure, preferably using a vacuum concentrator or a vacuum rotary evaporator, and drying is preferably using a reduced pressure drying, vacuum drying, boiling drying, spray drying or freeze drying method. However, the present invention is not limited thereto.

It is preferable to include the complex extract in an amount of 0.1 to 50% by weight based on the total weight of the composition containing the Schisandra leaf extract as an active ingredient of the present invention, but is not limited thereto.

The composition of the present invention may be administered in various oral and parenteral formulations during actual clinical administration. In the case of formulation, it can be prepared using diluents or excipients such as commonly used fillers, extenders, binders, wetting agents, disintegrants and surfactants.

Solid preparations for oral administration include tablets, pills, powders, granules, and capsules, and such solid preparations include at least one excipient in the pharmaceutical composition of the present invention, for example, starch, calcium carbonate, sucrose, It is prepared by mixing lactose and gelatin. In addition to simple excipients, lubricants such as magnesium, styrene, and talc may also be used.

Liquid formulations for oral administration include suspensions, solutions, emulsions, and syrups, and various excipients, such as wetting agents, sweeteners, fragrances, and preservatives, in addition to commonly used simple diluents such as water and liquid paraffin. have.

Formulations for parenteral administration include sterile aqueous solutions, non-aqueous solutions, suspensions, emulsions, freeze-dried preparations and suppositories. Non-aqueous solvents and suspensions may include propylene glycol, polyethylene glycol, vegetable oils such as olive oil, and injectable esters such as ethyl oleate. As the base of the suppository, witepsol, macrogol, Tween 61, cacao butter, laurin fat, glycerol and gelatin may be used. When administered parenterally, the pharmaceutical composition of the present invention may be administered through subcutaneous injection, intravenous injection or intramuscular injection.

The dosage of the pharmaceutical composition of the present invention varies depending on the condition and weight of the patient, the degree of disease, the drug form, the route and period of administration, and may be appropriately selected by those skilled in the art. However, for a desirable effect, the extract of the present invention is preferably administered at 0.1 to 1000 mg/kg per day. Administration may be administered once a day, or may be administered in several divided doses. However, it does not limit the scope of the present invention of the above dosage.

The composition of the present invention may be used alone or in combination with methods using surgery, hormone therapy, chemotherapy and biological response modifiers for the prevention and treatment of stroke or neurodegenerative disease.

In addition, the present invention provides a health functional food for preventing and improving stroke or neurodegenerative disease containing the leaf extract of Schisandra leaf as an active ingredient.

The health functional food of the present invention may be used as it is, or may be used in combination with other foods or food ingredients, and may be appropriately used according to a conventional method. The content of the active ingredient may be appropriately determined according to the purpose of use (prevention, health or therapeutic treatment). In general, in the production of food or beverage, the complex extract of the present invention may be added in an amount of 0.01 to 15% by weight based on the total weight of the food.

In addition, there is no particular limitation on the type of the food. Examples of foods to which the complex extract of the present invention can be added include beverages, gums, vitamin complexes, drinks, and the like, and include all health functional foods in a conventional sense.

The health functional food of the present invention may be a health functional drink, and the drink may contain various flavoring agents or natural carbohydrates as an additional component like a conventional drink. Examples of the natural carbohydrate include monosaccharides such as glucose, fructose and the like; disaccharides such as maltose, sucrose and the like; and polysaccharides such as conventional sugars such as dextrin, cyclodextrin, and the like, and sugar alcohols such as xylitol, sorbitol, and erythritol. In addition, flavoring agents (saccharin, aspartame, etc.) other than those described above can be used.

The health functional food of the present invention includes various nutrients, vitamins, minerals (electrolytes), flavoring agents such as synthetic and natural flavoring agents, coloring agents and enhancers (cheese, chocolate, etc.), pectic acid and its salts, alginic acid and salts thereof , organic acids, protective colloidal thickeners, pH adjusters, stabilizers, preservatives, glycerin, alcohol, carbonation agents used in carbonated beverages, and the like.

Schisandra leaf extract of the present invention reduces neuroinflammation, inhibits the activity of microglia, and has an excellent effect in protecting brain neurons, thereby preventing or treating stroke, Parkinson's disease and/or neurodegenerative disease It can be usefully used as a red composition or health functional food.

1 shows the results of confirming the weight loss inhibitory effect of Schisandra leaf extract treatment in an animal model of neuroinflammation.
2 shows the results of confirming the microglia activity inhibitory effect of Schisandra leaf extract treatment in an animal model of neuroinflammation.
3 shows the results of confirming the effect of inhibiting the expression of the microglia marker CD11b at the mRNA level according to the treatment of Schisandra leaf extract in an animal model of neuroinflammation.
4 shows the results of confirming the inhibitory effect on the expression of microglia markers CD11b and IBA-1 at the protein level according to the treatment of Schisandra leaf extract in an animal model of neuroinflammation.
5 shows the results of confirming the effect of inhibiting the expression of inflammatory factors on the mRNA level of Schisandra leaf extract treatment in an animal model of neuroinflammation.
6 shows the results of confirming the effect of inhibiting the expression of inflammatory factors at the protein level according to the treatment of Schisandra leaf extract in an animal model of neuroinflammation.

Hereinafter, the present invention will be described in more detail by way of Examples and Experimental Examples. However, the following examples are not intended to limit the scope of the present invention, which should be construed to aid the understanding of the present invention.

Example 1. Schisandra leaves (Leaves of Schisandra chinensis ) of hot water extract

200 g of dried omija leaves (Dongro-myeon, Mungyeong-si, Gyeongsangbuk-do) were put in a reflux extractor with 2.0 L of distilled water, left for 1.5 hours, and then heated for 1.5 hours from the point at which the broth started to boil. After the extract was filtered under reduced pressure with a filter paper, the filtrate was concentrated using a vacuum concentrator and a powder sample was prepared using a freeze dryer.

Example 2. Induction of neuroinflammation animal model using LPS (lipopolysaccharide)

In order to examine the anti-inflammatory effect of Schisandra leaf extract, an experimental neuroinflammation animal model was prepared by administering LPS. 8-9 weeks old male C57BL/6 mice (20-22g) (Nara Biotech Co., Ltd., Pyeongtaek) were prepared and stabilized for a week after birth, and then CON group (control group not administered with LPS and extract), LPS group (group administered by intraperitoneal administration of LPS 10 mg/kg), LPS + extract group (group administered intraperitoneally with LPS 10 mg/kg and oral administration of extract 50 mg/kg or 200 mg/kg), extract group (the group in which 200 mg/kg of the extract was administered orally) was divided. One hour prior to intraperitoneal administration of LPS, 100 μl of physiological saline was administered to the CON and LPS groups, and the extract was diluted in 100 μl of saline to the LPS + extract and extract groups and administered intraperitoneally.

Example 3. Confirmation of weight loss inhibitory effect in neuroinflammation model by LPS

Weight change was measured before and 24 hours after LPS administration using the animal model prepared in Example 2, and the results are shown in FIG. 1 .

As shown in FIG. 1 , it was confirmed that weight loss was inhibited in the LPS + extract group (LPS + LSC) compared to the LPS group.

Example 4. Confirmation of the effect of inhibiting microglia activation in a neuroinflammation model by LPS

24 hours after LPS administration, mice were anesthetized by inhalation with ether, perfusion-fixed with 4% paraformaldehyde (PFA) solution, and brains were removed and fixed in the same fixative for 24 hours. After washing the brain with PBS (phosphate buffered solution), it was stored in 30% sucrose solution for 2 days or more to prevent freeze damage. The cerebrum was cut into 30 μm thick using a cryosection and stored in PBS.

Immunostaining was performed using an antibody against IBA-1 (ionized calcium-binding adapter molecule-1) to confirm the degree of activation of microglia in the brain (indicating the degree of inflammatory response) at the protein level. Brain tissue cut to a thickness of 30 μm was immersed in PBS containing 3% hydrogen peroxide for 20 minutes to remove endogenous peroxidase activity, and washed with PBS. After immersing this in a blocking solution and reacting for 2 hours, it was reacted with IBA-1 antibody (1:2,000, WAKO, Japan), which is a marker of microglia, for one day at 4℃, washed with PBS, and then washed with the secondary antibody at room temperature. reacted for 1 hour. After the secondary antibody reaction, washing and dehydration, sealing with a permount (permount), and observed under a microscope.

The results are shown in FIG. 2 .

As can be seen in FIG. 2 , the LPS+extract group (LPS+LSC) showed that the activation degree of IBA-1 immunopositive microglia was significantly reduced compared to the LPS group.

In addition, in order to confirm the degree of activation of microglia at the mRNA level, the mRNA expression pattern for CD11b, a marker of microglia, was analyzed through reverse transcription-polymerase chain reaction (RT-PCR). . 24 hours after LPS administration, the mice were anesthetized by inhalation with ether, the cerebral cortex was extracted, 1 ml of Trizol (Trizol, Invitrogen, USA) was added, the tissue was ground with a grinder, and RNA was isolated by centrifugation. After synthesizing cDNA from the isolated RNA using the RT-PCR kit (Invitrogen, USA), 4 ul of cDNA and 1 ul of the microglia marker CD11b primer (Bionics, USA) were added to 1 ul and 2x SYBR GREEN (ABI) 5 ul, respectively. was measured and confirmed using real-time RT-PCR analysis using an ABI PRIAM 7500 instrument under the conditions of 50°C once for 2 minutes, 95°C once for 10 minutes, 95°C for 15 seconds, and 60°C for 1 minute 40 times.

The results are shown in FIG. 3 .

As shown in FIG. 3 , it was confirmed that the LPS + extract group (LPS + LSC) significantly reduced the level of CD11b mRNA expression increased by LPS compared to the LPS group.

In addition, a Western blot experiment was performed to confirm whether the extract inhibits the protein expression of CD11b and IBA-1, which are markers of microglia. 24 hours after LPS administration, the mice were anesthetized with ether by inhalation, and the cerebral cortex was removed and protein lysis buffer (50 mM Tris-cl, pH 7.5, 150 mM Nacl, 1% Triton X-100, 10) % glycerol and protease inhibitor mixture) was added to separate the protein. The isolated protein was quantified using the Bradford (Bio-rad, USA) method using bovine serum albumin (BSA, sigma, USA), and then 30 ug of the protein was subjected to 10% SDS-PAGE ( It was separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and transferred to a PVDF (polyvinylidene difluoride) membrane. The PVDF membrane was blocked in TBS-T (Tris-buffered saline, 20 mM Tris, pH 7.4, 0.1 % Tween 20 and 150 mM Nacl) containing 5% nonfat dry milk for 1 hour. After washing with TBS-T, the primary antibodies CD11b and Iba-1 (Millipore, USA) were diluted 1:1,000 and reacted at 4°C for one day. The reaction was carried out for 1 hour. After washing with TBS-T after the secondary antibody reaction, the band was confirmed with the ECL system (Amersham Pharmacia Biotechnology, USA).

The results are shown in FIG. 4 .

As can be seen in Figure 4, it was confirmed that the LPS + extract group (LPS + LSC) significantly reduced the protein expression of CD11b and IBA-1 increased by LPS compared to the LPS group.

Example 5. Confirmation of inhibitory effect on expression of inflammatory mediators in neuroinflammation model by LPS

A reverse transcription-polymerase chain reaction (RT-PCR) experiment was performed to determine whether the extract inhibits mRNA expression of inflammatory mediators. 24 hours after LPS administration, mice were anesthetized with ether by inhalation, the cerebral cortex was extracted, 1 ml of Trizol (Invitrogen, USA) was added, the tissue was ground with a grinder, and RNA was isolated by centrifugation. After synthesizing cDNA from the isolated RNA using an RT-PCR kit (Invitrogen, USA), 4 ul of cDNA and 1 ul of the microglia marker CD11b primer (Bionics, USA) were added to 1 ul and 2x SYBR GREEN (ABI) 5 ul, respectively. was measured and confirmed using real-time RT-PCR analysis using an ABI PRIAM 7500 instrument under the conditions of 50°C once for 2 minutes, 95°C once for 10 minutes, 95°C for 15 seconds, and 60°C for 1 minute 40 times.

The results are shown in FIG. 5 .

As confirmed in Figure 5, the LPS + extract group (LPS + LSC) compared to the LPS group inflammatory cytokines (TNF-α, IL-1β, IL-6) increased by LPS mRNA expression levels of iNOS and COX2 was found to significantly decrease.

In addition, a Western blot experiment was performed to confirm whether the extract inhibits the protein expression of inflammatory mediators. 24 hours after LPS administration, the mice were anesthetized with ether by inhalation, and the cerebral cortex was removed and protein lysis buffer (50 mM Tris-cl, pH 7.5, 150 mM Nacl, 1% Triton X-100, 10) % glycerol and protease inhibitor mixture) was added to separate the protein. The isolated protein was quantified using the Bradford (Bio-rad, USA) method using bovine serum albumin (BSA, sigma, USA), and 30 ug of the protein was subjected to 10% SDS-PAGE ( It was separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and transferred to a PVDF (polyvinylidene difluoride) membrane. The PVDF membrane was blocked in TBS-T (Tris-buffered saline, 20 mM Tris, pH 7.4, 0.1 % Tween 20 and 150 mM Nacl) containing 5% nonfat dry milk for 1 hour. After washing with TBS-T, the primary antibodies iNOS and COX-2 (Millipore, USA) were diluted 1:1,000 and reacted at 4°C for one day, then washed 3 times with TBS-T for 10 minutes each and at room temperature with the secondary antibody The reaction was carried out for 1 hour. After washing with TBS-T after the secondary antibody reaction, the band was confirmed with the ECL system (Amersham Pharmacia Biotechnology, USA).

The results are shown in FIG. 6 .

6, it was confirmed that the LPS + extract group (LPS + LSC) significantly reduced the expression of COX-2 and iNOS increased by LPS compared to the LPS group.

Formulation Example 1. Preparation of pharmaceuticals

1.1 Preparation of powders

The above ingredients are mixed and filled in an airtight bag to prepare a powder.

1.2 Preparation of tablets

After mixing the above ingredients, tablets are prepared by tableting according to a conventional manufacturing method of tablets.

1.3 Preparation of capsules

According to a conventional capsule preparation method, the above ingredients are mixed and filled in a gelatin capsule to prepare a tablet.

1.4 Preparation of liquid formulations

Purified water was added to adjust the total volume to 100 ml. After mixing the above ingredients according to a conventional liquid preparation method, it is filled in a brown bottle and sterilized to prepare a liquid preparation.

Formulation Example 2. Preparation of health functional food

The composition ratio of the vitamin and mineral mixture is relatively suitable for health functional food, but the composition is mixed in a preferred embodiment, but the mixing ratio may be arbitrarily modified, and the above ingredients are mixed according to a conventional health functional food manufacturing method. Then, according to a conventional method, it can be used for manufacturing a health functional food composition (eg, nutritional candy, etc.).

Formulation Example 3. Preparation of health functional beverage

After mixing the above ingredients according to the usual health functional beverage manufacturing method, after stirring and heating at 85°C for about 1 hour, the resulting solution is filtered and obtained in a sterilized 2ℓ container, sealed and sterilized, then refrigerated. It is used to prepare the health functional beverage composition of the present invention.

Although the composition ratio is prepared by mixing ingredients suitable for relatively favorite beverages in a preferred embodiment, the mixing ratio may be arbitrarily modified according to regional and national preferences such as demand class, demanding country, and use.

Claims (6)

Contains Schisandra leaf hot water extract as an active ingredient,
The extract is extracted using water as an extraction solvent,
The Schisandra leaf hot water extract is extracted by mixing the Schisandra leaf and the extraction solvent in a weight ratio of 1:10,
As a pharmaceutical composition for the prevention or treatment of stroke or neurodegenerative disease,
The stroke or degenerative neurological disease has increased expression of IBA-1, a microglial cell activating factor, and increased expression of CD11b, a microglia marker, in the group consisting of TNF-α, IL-1β and IL-6. A composition, characterized in that the selected inflammatory factor is increased stroke or neurodegenerative disease. According to claim 1, wherein the degenerative neurological disease is stroke, dementia, Alzheimer's disease, Parkinson's disease, Huntington's disease, Pick's disease, Creutzfeldts-Jakob disease, frontotemporal dementia, Lewy dementia, muscular atrophic lateral sclerosis, cortical basal degeneration, multiple systems Atrophy, progressive supranuclear palsy, nervous system autoimmune disease, inflammatory and neuropathic pain, and a pharmaceutical composition for the prevention or treatment of any one selected from the group consisting of cerebrovascular disease, stroke or neurodegenerative disease. The pharmaceutical composition for preventing or treating stroke or neurodegenerative disease according to claim 2, wherein the neurodegenerative disease is Parkinson's disease. Contains Schisandra leaf hot water extract as an active ingredient,
The extract is extracted using water as an extraction solvent,
The Schisandra leaf hot water extract is extracted by mixing the Schisandra leaf and the extraction solvent in a weight ratio of 1:10,
As a health functional food for the prevention or improvement of stroke or neurodegenerative disease,
The stroke or degenerative neurological disease has increased expression of IBA-1, a microglial cell activating factor, and increased expression of CD11b, a microglia marker, in the group consisting of TNF-α, IL-1β and IL-6. A health functional food, characterized in that the selected inflammatory factor is increased stroke or neurodegenerative disease. 5. The method of claim 4, wherein the neurodegenerative disease is stroke, dementia, Alzheimer's disease, Parkinson's disease, Huntington's disease, Pick's disease, Creutzfeldt-Jakob disease, frontotemporal dementia, Lewy dementia, muscular atrophic lateral sclerosis, cortical basal degeneration, multiple systems A health functional food for the prevention or improvement of any one selected from the group consisting of atrophy, progressive supranuclear palsy, nervous system autoimmune disease, inflammatory and neuropathic pain, and cerebrovascular disease. According to claim 5, wherein the neurodegenerative disease is Parkinson's disease, a health functional food for preventing or improving stroke or neurodegenerative disease.

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