WO2018080157A1 - Composition for preventing, improving or treating cognitive impairment, containing ficus erecta extract as active ingredient - Google Patents

Abstract

The present invention relates to a composition for preventing, improving or treating cognitive impairment, the composition containing a Ficus erecta extract as an active ingredient, and more specifically, the Ficus erecta extract, according to the present invention, exhibits antioxidant activity, amyloid-beta aggregation inhibition activity, a nerve cell protection effect and a brain cell inflammation inhibition effect, and thus may be usefully employed as a composition for preventing, improving or treating cognitive impairment.

Description

Composition for the prevention, improvement or treatment of cognitive impairment containing cheonnyeong fruit tree extract as an active ingredient

The present invention is a ficus tree ( Ficus) e recta ) relates to a composition for the prevention, improvement or treatment of cognitive impairment containing the extract as an active ingredient.

Cognition refers to all processes in which humans use their brains to think, speak, remember, judge, and execute. Therefore, 'cognitive function' includes attention, perception, memory, language ability, executive ability, etc., 'cognitive impairment' is the most prominent phenomenon of the aging of the brain, characterized by a decrease in learning, memory, and judgment It is a physiological phenomenon that is erased. In particular, these cognitive impairments may appear in various ways. Among them, dementia is markedly impaired in interpersonal relations, occupational functions, and daily life functions due to the decline in cognitive functions such as memory, language skills, visual perception and space-time composition ability, and executive functions. It is diagnosed as a complex disease that results. Geriatric dementia is mainly caused by Alzheimer's dementia. Alzheimer's dementia is commonly referred to as Alzheimer's disease (AD), and it can be said to die slowly without any treatment efforts. The disease was known in 1906 by Alois Alzheimer, a German neuropathologist. In 1960, the elderly population of 72 million people was 720,000 in 1960, accounting for only 2.9%, but it is expected to become a full-fledged aging society, and after 2026, the population aged 65 or older will increase to 20% of the total population. . The number of patients with senile dementia increases sharply in proportion to this. Experts predict that 10% of people over 65 years of age will suffer from senile dementia, and 40% to 50% of people over 85 years of age.

Cognitive dysfunction, such as the loss of memory and learning ability caused by Alzheimer's disease (AD), a type of senile dementia, is caused by the aggregation and deposition of two insoluble proteins in the hippocampus and cortex. Protein aggregation is the accumulation of neurofibrillary tangles consisting of senile plaque composed of amyloid beta (Aβ) and hyperphosphorylated tau protein in neurons. Despite many efforts, the cause and invention of Alzheimer's disease are still not fully understood. As the aging population is accelerating, the demand for the development of more effective formulations (including health functional food ingredients) to improve cognitive or memory decline is more than ever. As a result, there is a need for research to develop a referral having a new multi-functional effect in the mechanism of neuronal cells for the development of dementia.

On the other hand, cheonseondae and trees grow at the foot of the seashore, the height of 2 ~ 4m, the bark is flat, the branches are off-white, milky juice comes out when the wound is cut out, leaves are oval-shaped, the egg is upside down, and the edge is flat. to be. Lateral veins 5 ~ 6 pairs, 8 ~ 17cm long, surface green, hairy, light brown. Petiole is 1-4cm long. Flowers bloom in May-June, single flowers, with one flower spike on the axilla of the new branch. At the end of the stalk there is a round fruit-like cyst and there are three artillery just below. The capsule is about 15mm in diameter and contains many flowers inside. A male flower has 5 to 6 branched pieces and 3 stamens, and a female flower has 3 to 5 branched pieces and 1 pistil. The capsule grows into fruit and becomes 15 ~ 17mm in diameter and can be eaten when it is cooked black in August ~ September. Seeds are egg-shaped, about 1.6mm long. It was named after the fruits of heavenly elves. It is distributed in Korea, Japan, and China.

As an example of a technique related to cheongiwa tree extract, Chinese Patent Publication No. 104998174 discloses a method for preventing, improving or treating cerebral atrophy comprising an herbal medicine composition comprising right roots of roots of cheongiwa tree as an active ingredient. , Korean Patent No. 1042718 discloses a cosmetic composition having anti-aging or skin lightening activity containing a cheonnyang and leaf extract, and IL-6 and COX- which is a subject of osteoporosis reaction in Korean Patent No. 0694570 2 discloses a composition for the prevention and treatment of osteoporosis, including narrow leaf scabs and extracts and fractions exhibiting expression suppression, but the prevention, improvement or There is no disclosure of therapeutic compositions.

The present invention is derived from the above requirements, relates to a composition for the prevention, improvement or treatment of cognitive impairment containing an extract of Aspen as an active ingredient, the amyloid beta aggregation inhibition, antioxidant activity of the Aspen extract The present invention was completed by confirming neuroprotective and anti-inflammatory effects of brain cells.

In order to achieve the above object, the present invention provides a pharmaceutical composition for the prevention or treatment of cognitive impairment containing cheonnyeongwa tree extract as an active ingredient.

In another aspect, the present invention provides a health functional food composition for the prevention or improvement of cognitive impairment containing cheonnung fruit tree as an active ingredient.

The present invention relates to a composition for the prevention, improvement or treatment of cognitive impairment, containing aspen as an active ingredient, the aspen extract inhibits amyloid beta aggregation, antioxidant activity, nerve cell protection and brain cell inflammation Since it is effective, it can be used for the prevention, improvement or treatment of cognitive impairment.

Figure 1 confirms the inhibitory effect of amyloid beta coagulation of the cheongiwa extract of the present invention, (A) is the amyloid beta leaf extract, (B) confirms the amyloid beta aggregation inhibitory effect of cheongiwa branch extract, positive As a control, 100 μM of Morin compound was used.

Figure 2 confirms the antioxidant activity of the cheonnyeongpo tree extract of the present invention, (A) is the result of confirming the ABTS radical scavenging activity of the cheonnungpo tree leaf extract, (B) is the DPPH radical scavenging activity of the cheonnung tree leaf extract (C) is the result of confirming the ABTS radical scavenging activity of the Tsunami branches and (D) is the result of confirming the DPPH radical scavenging activity of the Tsunami branches. Vitamin C (vit. C) was used as a positive control.

Figure 3 confirms the neuronal protective effect (CCK) of the cheongiwa tree leaf extract of the present invention, (A) in order to confirm the cytotoxicity to the neuronal hippocampal cell line, treated cheongiwa tree leaf extract and cell survival rate and check result, (B) is the result confirming the cytoprotective effect by treating the cheonseon and leaf extract on the neuronal cell is induced neuronal damage by handling the H ₂ O _2, (C) the LDH leakage due to cell membrane damage Cell viability was measured through the measurement of. ## and ### are statistically significant differences in cell survival rate or LDH release due to neuronal damage following H ₂ O ₂ treatment, compared to the normal group. ### means p <0.001. *, **, *** is compared with the H ₂ O ₂ treatment group, the survival rate of the neurons or LDH release by the treatment of cheongiwa tree leaf extract statistically significant difference, * is p <0.05 And ** is p <0.01 and *** means p <0.001.

Figure 4 as a result of confirming the inhibitory effect on the brain cell inflammation according to the treatment of the extract of the senile gland of the present invention, (A) is the result of confirming the toxicity of microglia cells, (B) is the inflammation to BV-2 cells After induction, the result of NO assay according to the treatment of cheongibana leaf extract, (C) is the result of PGE ₂ assay according to the treatment of cheongibana leaf extract after inducing inflammation in BV-2 cells. ### means that the production of nitric oxide (NO) or PGE ₂ was significantly increased by damage to neurons following LPS treatment, which means p <0.001. *** indicates that NO (nitric oxide) or PGE ₂ production was statistically significantly decreased by treatment with the extract of L. japonicum compared to LPS treatment group, *** means p <0.001.

The present invention relates to a pharmaceutical composition for the prevention or treatment of cognitive impairment, containing aspen active extract.

The cheonnyeongwa tree extract may be prepared by a method comprising the following steps, but is not limited thereto:

1) extracting by adding an extraction solvent to the cheonnyeongwa tree plant;

2) filtering the extract of step 1); And

3) concentration of the filtered extract of step 2) under reduced pressure and drying to prepare an extract.

The extraction solvent in step 1) is preferably water, a lower alcohol of C ₁ ~ C ₄ or a mixture thereof, more preferably an ethanol extract, even more preferably 70% (v / v) ethanol ultrasonic extract It is not limited to this.

In the above production method, the extraction of the cheonnyeongwa tree can use all conventional methods known in the art, such as filtration, hot water extraction, immersion extraction, reflux cooling extraction and ultrasonic extraction. The extraction solvent is preferably extracted by adding 1 to 20 times the volume of dried Cheonsun and wood, and more preferably 3 to 10 times. Extraction temperature is preferably 20 to 50 ℃ but is not limited thereto. In addition, the extraction time is preferably 0.5 to 10 hours, more preferably 0.5 to 5 hours, most preferably 1 hour is not limited thereto. In the above method, the reduced pressure concentration in step 3) is preferably a vacuum reduced pressure concentrator or a vacuum rotary evaporator, but is not limited thereto. In addition, the drying is preferably reduced pressure drying, vacuum drying, boiling drying, spray drying or freeze drying, but is not limited thereto.

The cheongiwa extract may be an extract of an outpost, a flower, a leaf, a branch, a root or a seed, but is preferably an extract of a leaf or a branch of the cheonnabi.

The cognitive impairment is preferably any one selected from dementia, Alzheimer's, ischemic stroke, traumatic brain injury, forgetfulness, Parkinson's disease, pick disease, Creutzfeldt-Jakob disease, and mild cognitive impairment Do not.

In the present invention, mild cognitive impairment is defined as a pre-dementia clinical stage that does not cause a state in which memory and cognitive function is significantly lower than age and education level or disruption in life.

The composition of the present invention may include a pharmaceutically acceptable carrier, excipient or diluent in addition to the active ingredient, and may be various oral or parenteral formulations. When formulated, diluents or excipients such as fillers, extenders, binders, wetting agents, disintegrating agents, and surfactants are usually used. Solid preparations for oral administration include capsules, powders, granules, tablets, pills, and the like, which may comprise at least one excipient such as starch, calcium carbonate, sucrose or lactose (at least one compound). lactose) and gelatin. In addition to simple excipients, lubricants such as magnesium stearate, talc and the like are also used. Liquid preparations for oral administration include suspensions, emulsions, syrups, aerosols and the like, and may include various excipients such as wetting agents, sweeteners, fragrances, preservatives, etc., in addition to commonly used simple diluents such as water and liquid paraffin. Formulations for parenteral administration include sterile aqueous solutions, non-aqueous solvents, suspensions, emulsions, lyophilized preparations, suppositories. As the non-aqueous solvent and the suspension solvent, propylene glycol, polyethylene glycol, vegetable oil such as olive oil, injectable ester such as ethyl oleate, and the like can be used. As the base of the suppository, witepsol, macrogol, tween 61, cacao butter, laurin butter, glycero gelatin and the like can be used. For parenteral administration, it is desirable to select either external skin or intraperitoneal, rectal, intravenous, intramuscular, subcutaneous, intrauterine dural or cerebrovascular injections, most preferably for external skin use.

The pharmaceutical composition according to the invention is administered in a pharmaceutically effective amount. In the present invention, "pharmaceutically effective amount" means an amount sufficient to treat a disease at a reasonable benefit / risk ratio applicable to medical treatment, the effective amount of the level of the disease, the severity, the drug activity of the patient , Sensitivity to the drug, time of administration, route of administration and rate of release, duration of treatment, factors including concurrent use of the drug, and other factors well known in the medical arts. The compositions of the present invention may be administered as individual therapeutic agents or in combination with other therapeutic agents, may be administered sequentially or simultaneously with conventional therapeutic agents, and may be single or multiple doses. Taking all of the above factors into consideration, it is important to administer an amount that can achieve the maximum effect with a minimum amount without side effects, which can be readily determined by one skilled in the art.

The dosage of the composition of the present invention varies depending on the weight, age, sex, health status, diet, time of administration, administration method, excretion rate and severity of the disease of the patient, the daily dosage is the amount of extract 0.01 to 2,000 mg / kg, preferably 30 to 500 mg / kg, more preferably 50 to 300 mg / kg, can be administered 1 to 6 times a day. The compositions of the present invention can be used alone or in combination with methods using surgery, radiation therapy, hormone therapy, chemotherapy and biological response modifiers.

The present invention also relates to a health functional food composition for the prevention or improvement of cognitive impairment containing cheonnung fruit tree extract as an active ingredient. The composition is characterized by having antioxidant activity, the composition is preferably prepared in any one of the formulations selected from powders, granules, pills, tablets, capsules, candy, syrups and beverages, but is not limited thereto.

In the case of using the health functional food composition of the present invention as a food additive, the cheonnyeongwa tree extract 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 blending amount of the active ingredient can be suitably determined according to the purpose of its use (prevention, health or therapeutic treatment). Generally, in the preparation of food or beverages, the composition of the present invention is added in an amount of up to 15 parts by weight, preferably up to 10 parts by weight based on the raw materials. However, in the case of long-term intake for health and hygiene or health control purposes, 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 foods to which the extract or fractions thereof may be added include dairy products including meat, sausage, bread, chocolate, candy, snacks, confectionery, pizza, ramen, other noodles, gum, ice cream, various soups, drinks, tea , Drinks, alcoholic beverages and vitamin complexes, and includes all the health functional foods in the conventional sense.

When the composition of the present invention is used as a health beverage, various flavors, natural carbohydrates, and the like may be contained as additional components, as in general beverages. The above-mentioned natural carbohydrates are sugars such as monosaccharides such as glucose and fructose, disaccharides such as maltose and sucrose, polysaccharides such as textine and cyclotenstrin, 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 g of the composition of the present invention. In addition to the above, the composition of the present invention includes various nutrients, vitamins, electrolytes, flavors, coloring agents, pectic acid and salts thereof, alginic acid and salts thereof, organic acids, protective colloidal thickeners, pH adjusting agents, stabilizers, preservatives, glycerin, alcohols. And carbonation agents used in carbonated 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 the composition of the present invention is generally selected in the range of 0.01 to 0.1 parts by weight per 100 parts by weight.

Hereinafter, the present invention will be described in more detail with reference to Examples. These examples are only for explaining the present invention in more detail, it is obvious to those skilled in the art that the scope of the present invention is not limited by them.

1. Preparation method of extract

Cheonsei Aster leaves and branches were used from the Medicinal Plant Material Bank of Gachon University. 5 L of 70% (v / v) ethanol was added to 500.0 g of each dried sample and the leaves and branches of the periwinkle and ultrasonically extracted three times for 1 hour using an ultrasonic extractor. The ultrasonic extract was filtered using Advantec No. 2 (110 mm) filter paper to remove insoluble matters, and then concentrated under reduced pressure at 40 ° C. with a condenser equipped with a cooling condenser. To completely remove the solvent of the concentrated extract under reduced pressure, 500 ml of purified water was added and suspended, and then concentrated by using a lyophilizer.

2. Determination of the Effect of Amyloid Beta Aggregation Inhibition

Amyloid beta aggregation inhibitory activity was measured by fluorescence assay. Amyloid beta (Aβ _1-42 ) peptide was stored at minus 80 ℃, the final concentration used in the measurement was used to 100㎛ / ㎖. Thioflavin T, used as a fluorescent substance, was dissolved in assay buffer (50 mM Tris / 150 mM NaCl (pH 7.2), 20 mM HEPES / 150 mM NaCl (pH 7.2), 10 mM phosphate / 150 mM NaCl (pH 8.0)). It was prepared and used at a concentration of 2 mM. Samples were dissolved in assay buffer and used at a final concentration of 100 μg / ml. In order to measure the degree of Aβ _1-42 aggregation, 10 μl of thioflavin T and 85 μl of Aβ _1-42 were added to a 96-well plate and mixed with 5 μl of a sample prepared at a constant concentration. Measured with a spectrometer. The wavelength value of the fluorescence spectrometer used at this time was 440 nm / 484 nm (absorption / emission), and it measured in total for 2 hours at 37 degreeC 20 minutes. Morin compounds were used as positive controls for activity comparison.

3. Antioxidant Activity Assay

(A) Determination of ABTS free radical scavenging ability

Antioxidant efficacy measurement using ABTS (2,2'-azino-bis (3-ethylbenzothiazoline-6-sulphonic acid)) radical was carried out by modifying the ABTS + cation decolorization assay method to 96 well plates. 7 mM ABTS and 2.45 mM potassium persulfate were mixed at the final concentration and left for 24 hours in the dark at room temperature to form ABTS +. And diluted with PBS to have an absorbance value of 0.7 at 743 nm. After mixing ABTS + solution and the sample in a 96 well plate and reacting at room temperature for 30 minutes, the absorbance was measured at 743 nm using an Epoch Microplate Spectophotometer. The radical scavenging activity of each sample was expressed as a percentage of the radical scavenging ability with respect to the control group using PBS as a control group. Vitamin C (vit. C) was used as a positive control for activity comparison.

(B) Measurement of DPPH free radical scavenging ability

Antioxidant potency measurements using DPPH (1-1-diphenyl-2-picrylhydrazyl) radicals were performed using 96 well plates. 0.15 mM DPPH solution and the sample were mixed in a 96 well plate and reacted at room temperature for 30 minutes, and then the absorbance was measured at 517 nm. The antioxidant activity of each treatment extract was expressed as a percentage of radical scavenging ability with respect to the control group using the solvent DMSO as a control. Vitamin C (vit. C) was used as a positive control for activity comparison.

4. Measurement of neuronal protective effect

(A) Cytotoxicity measurements on neuronal hippocampal cell lines

In order to determine the cytotoxicity of the sample, Cell Counting Kit-8 (CCK-8) was used according to the manufacturer's instructions. Samples were treated by concentration in HT22 cell lines (5 × 10 ³ cells / well) dispensed in 96-well plates and incubated for 24 hours. After incubating for 4 hours with 10 μl of CCK-8 solution, absorbance was measured at 450 nm and relative cell viability (% of control) was calculated by comparison with the control group.

(B) Measurement of neuronal cell protective efficacy

In order to induce neuronal damage, HT22 cells were treated with 250 μM hydrogen peroxide (H ₂ O ₂ ) for 6 hours. H ₂ O ₂ via CCK Assay The cell protection efficacy was determined by comparing the change in cell viability of the treatment group alone and the sample and H ₂ O ₂ simultaneous treatment group. Carvedilol was used as a positive control.

(C) LDH assay

Cell viability was measured by measuring LDH efflux due to cell membrane damage. In order to induce nerve cell damage, HT22 cells were treated with 250 μM of hydrogen peroxide (H ₂ O ₂ ) for 6 hours. After the culture supernatant was collected, the mixture was mixed with the LDH substrate solution in the same amount and reacted at room temperature for 30 minutes. Then, 1N HCl was added to stop the reaction, and the absorbance was measured at 490 nm (experimental LDH release).

After removing the supernatant, lysis solution was added to the remaining cells and reacted at 37 ° C. for 45 minutes, followed by centrifugation at 250 g for 4 minutes. The supernatant was collected and subjected to LDH reaction as described above to measure absorbance at 490 nm (Maximum LDH release). Cell viability was calculated by the following equation (1).

Formula (1)

% Cell survival rate = {[experimental LDH release (OD ₄₉₀ )] / [Maximum LDH release (OD ₄₉₀ )]} × 100

5. Inhibition of brain cell inflammation

(A) Determination of microglial toxicity

Samples were treated by concentration in BV-2 cell lines (1 × 10 ⁴ cells / well) dispensed in 96-well plates and incubated for 24 hours. After incubating for 4 hours with 10 μl of CCK-8 solution, absorbance was measured at 450 nm and relative cell viability (% of control) was calculated by comparison with the control group.

(B) NO (nitric oxide) assay

After pretreatment with BV-2 cells for 2 hours, LPS (lipopolysaccharide, 1 µg / ml) was treated and cultured for 24 hours to induce an inflammatory response, and then the supernatant was recovered. After 5-10 minutes of reaction with the same amount of the supernatant and Griess reagent (sulfanilamide: N- 1-napthylethylenediamine dihydrochloride = 1: 1), the absorbance at 540 nm was measured to calculate the amount of nitric oxide (NO) based on the standard curve. . Ibuprofen (ibuprofen) was used as a positive control.

(C) PGE ₂ (Prostaglandin E ₂ ) Assay

After pretreatment of the sample to BV-2 cells for 2 hours, in order to induce an inflammatory response, LPS (lipopolysaccharide, 1㎍ / ㎖) was treated and incubated for 24 hours, and then the supernatant was recovered. Experiments were performed using an enzyme-linked immunosorbent assay (ELISA) kit to measure the amount of PGE ₂ in cell culture. The supernatant was added to a 96-well plate coated with goat anti-mouse IgG, 50 μl each, and 50 μl of the primary antibody solution and 50 μl of PGE ₂ conjugate were added thereto, and reacted at 4 ° C. for 18 hours. After washing 5 times with a washing buffer and 200μL reaction of the substrate solution was reacted for 90 minutes, the absorbance was measured at 412nm.

Example  One. Zenith and tree  Confirmation of the Amyloid-beta Aggregation Inhibitory Effect of Extracts

6.25, 12.5, 25, 50, and 100 ㎍ / ㎖ senile and leaf and eggplant extracts were treated to determine the degree of aggregation inhibition of amyloid beta. As a result, as shown in FIG. 1, the T. herb leaf extract inhibited amyloid beta aggregation in a concentration-dependent manner, and when the 50 µg / ml T. herb extract was treated, the inhibition of amyloid beta aggregation was about 60%. And, when treated with 100 ㎍ / ㎖ Celtic leaves extract, it was confirmed that the inhibition of amyloid beta aggregation is about 60% or more. On the other hand, 100 ㎍ / ㎖ bark branch extract showed 35-40% amyloid beta aggregation inhibition.

Example  2. Zenith and tree  Confirmation of Antioxidant Activity of Extracts

In Example 2, ABTS radical scavenging activity and DPPH radical scavenging activity were confirmed in order to confirm the antioxidant activity of the T. olecus leaf and eggplant extract. As shown in FIG. Radical scavenging activity and DPPH radical scavenging activity were observed, and the extracts of T. vulgaris showed similar effects as ABTS radical scavenging activity, but the DPPH radical scavenging activity was hardly exhibited.

Example  3. Zenith and tree  Confirmation of neuroprotective effect of extract

In Example 3, it was confirmed that the extract of the celestial nectar has little cytotoxicity against normal neurons (FIG. 3 (A)), and due to H ₂ O ₂ damage to neurons, cell viability was reduced, and H It was confirmed that there is an effect of suppressing a decrease in cell viability by treating neural cell damage caused by ₂ O ₂ damage to the celestial azalea leaf extract (FIG. 3 (B)).

In addition, LDH release was increased due to damage to the cell membrane of H ₂ O ₂ neurons, but the effect of mitigating the increase in LDH release was confirmed by treating the celestial arachnid leaf extract (FIG. 3 (C)).

Example  4. Confirmation of inhibitory effect on brain cell inflammation

In Example 4, it was confirmed that the inhibitory effect on brain cell inflammation, and as a result, as shown in FIG. . Induction of inflammation in brain cells by treatment with LPS increased NO (nitric oxide) production, but when treated with the extract of the bark of the present invention, NO (nitric oxide) production significantly decreased, in particular, 100 In the case of treatment of periwinkle nectar leaves extract, NO (nitric oxide) production was hardly produced.

In addition, as a result of measuring the amount of PGE _{2 in the} cell culture, it was confirmed that the amount of PGE ₂ increased when the inflammation was induced, whereas the amount of PGE ₂ was decreased in the treatment group of the TPS extract compared to the LPS treatment group.

Claims (10)

Celestial Tree and Ficus e recta ) Pharmaceutical composition for the prevention or treatment of cognitive impairment containing the extract as an active ingredient. [Claim 2] The pharmaceutical composition for preventing or treating cognitive impairment according to claim 1, wherein the extract is a leaf or branch extract of the celticus. The pharmaceutical composition for preventing or treating cognitive impairment according to claim 1, wherein the solvent of the cheongidaewa extract is water, C ₁ ~ C ₄ lower alcohol, or a mixture thereof. The method of claim 1, wherein the cognitive impairment is any one selected from dementia, Alzheimer's disease, ischemic stroke, traumatic brain injury, forgetfulness, Parkinson's disease, pick disease, Crutzfeldt-Jakob disease and mild cognitive impairment. Pharmaceutical composition for the prevention or treatment of cognitive disorders, characterized in that. The pharmaceutical composition for preventing or treating cognitive impairment according to claim 1, comprising a pharmaceutically acceptable carrier, excipient or diluent in addition to the active ingredient. According to claim 1, wherein the composition is a capsule, powder, granules, tablets, suspensions, emulsions, syrups, aerosol pharmaceutical composition for the prevention or treatment of cognitive impairment, characterized in that it is prepared in any one of the formulations. Health functional food composition for the prevention or improvement of cognitive impairment containing cheonseon fruit extract as an active ingredient. 8. The health functional food composition for preventing or improving cognitive impairment according to claim 7, wherein the solvent of the cheongiwa fruit extract is water, a lower alcohol of C ₁ to C ₄ or a mixture thereof. 8. The health functional food composition for preventing or improving cognitive impairment according to claim 7, wherein the composition has antioxidant activity. According to claim 7, wherein the composition is a health functional food composition for the prevention or improvement of cognitive impairment, characterized in that the formulation is made of any one selected from powder, granules, pills, tablets, capsules, candy, syrups and beverages.

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