ANTI-ALZHEIMER COCONUT SPROUT EXTRACT COMPOSITION FOR COGNITIVE AND MEMORY ENHANCEMENT

Abstract

The present invention relates to a pharmaceutical composition comprising a coconut sprout extract (Cocos nucifera) combined with additional active ingredients to enhance cognitive function and mitigate symptoms of neurodegenerative disorders, specifically Alzheimer’s disease. The composition includes synergistic natural compounds, such as trigonelline, along with controlled dosages of donepezil, to provide neuroprotection through mechanisms of antioxidant, anti-inflammatory, and cholinergic enhancement. Animal models demonstrate that this formulation significantly improves memory retention and cognitive function by modulating acetylcholinesterase activity, reducing oxidative stress, and enhancing neurotransmitter levels. The composition is formulated for oral administration and maintains stability through the inclusion of appropriate excipients and preservatives.

Specification

Description:ANTI-ALZHEIMER COCONUT SPROUT EXTRACT COMPOSITION FOR COGNITIVE AND MEMORY ENHANCEMENT

FIELD OF THE INVENTION
The present invention relates to the field of neuropharmacology and herbal medicine, particularly to compositions derived from natural sources aimed at treating cognitive impairments associated with Alzheimer's disease (AD). More specifically, the present invention focuses on enabling Coconut Sprout Extract (CSE), as a neuroprotective agent capable of enhancing memory and cognitive function.

BACKGROUND OF THE INVENTION
Alzheimer's disease (AD) represents a significant and growing public health concern worldwide, characterized by progressive cognitive decline, memory impairment, and personality changes. The pathological hallmarks of AD include the accumulation of amyloid-beta (Aß) plaques, neurofibrillary tangles composed of hyperphosphorylated tau protein, and significant neuronal loss in critical brain regions such as the hippocampus and the cornus ammonis (CA1) subfield. The underlying mechanisms leading to AD involve complex interactions among genetic, environmental, and lifestyle factors, contributing to oxidative stress, neuroinflammation, and cholinergic deficits.

Conventional treatments for AD primarily focus on symptom management rather than addressing the underlying disease pathology. Acetylcholinesterase inhibitors (AChEIs), such as Donepezil, are widely used to enhance cognitive function by preventing the breakdown of acetylcholine, a neurotransmitter crucial for learning and memory. However, these synthetic drugs often come with adverse side effects, including gastrointestinal disturbances and cardiovascular issues, which limit their long-term use and effectiveness.
The search for alternative therapies has prompted interest in natural compounds with neuroprotective properties. Phytochemicals derived from plants have been recognized for their ability to enhance cognitive function, combat oxidative stress, and exhibit anti-inflammatory effects. In this regard, the Coconut Sprout Extract (CSE) has emerged as a promising candidate, given its rich phytochemical profile, including flavonoids, saponins, phenolic acids, and vitamins. These constituents are known to confer neuroprotective effects and may play a crucial role in modulating the biochemical pathways implicated in AD.
The present invention presents a formulation of CSE, validated through rigorous preclinical testing in Swiss Albino mice (SAM) models, demonstrating significant improvements in cognitive function and memory enhancement through various behavioral and biochemical assessments. The formulation aims to provide a natural, effective therapeutic option for AD, targeting key pathological processes associated with the disease.
Further, the present invention addresses the need for effective, natural alternatives or adjuncts to conventional Alzheimer's therapies that can mitigate the neurodegenerative processes associated with the disease, improve the quality of life for affected individuals, and reduce the burden of existing pharmacological interventions.

OBJECTIVE OF THE INVENTION
The primary objective of the invention is to develop a novel pharmaceutical composition comprising coconut sprout extract (Cocos nucifera) in combination with trigonelline, donepezil, and other natural compounds, aimed at providing neuroprotection and mitigating symptoms associated with neurodegenerative conditions, particularly Alzheimer's disease. The invention seeks to harness the antioxidant, anti-inflammatory, and cholinergic properties of these compounds to support cognitive function, enhance memory retention, and reduce oxidative stress.
This composition offers a plant-based therapeutic alternative to existing Alzheimer's treatments by addressing both the physiological and biochemical pathways involved in cognitive decline. Additionally, the invention aims to ensure stability, bioavailability, and ease of administration, making it suitable for long-term use in managing cognitive impairment and enhancing overall brain health.

BRIEF DESCRIPTION OF THE DRAWINGS
The accompanying figures illustrate several embodiments of the disclosure and, together with the description, serve to explain the principles of the disclosure. One of ordinary skill in the art readily recognizes that the embodiments illustrated in the figures are merely exemplary, and are not intended to limit the scope of the present disclosure.
FIG. 1 illustrates an exemplary diagrammatic representation of an exemplary experimental hypothesis of the present disclosure.
FIG. 2 illustrates an exemplary diagrammatic representation of an exemplary experimental protocol of the present disclosure.
FIG. 3 (A) discloses effect of CSE on Escape latency by using Morris Water Maze.
FIG. 3 (B) discloses treatment effect of CSE on Percentage alteration by using Y Maze.
FIG. 4 discloses CSE decreases acetylcholinesterase level in scopolamine induced Alzheimer's in subjects.
FIG. 5 discloses CSE increased Catalase level in scopolamine induced Alzheimer's in subjects.
FIG. 6 discloses CSE increased level of GSH in scopolamine induced Alzheimer's in subjects.
FIG. 7 discloses CSE decreased MDA level in scopolamine induced Alzheimer's in subjects.
Further areas of applicability of the present disclosure will become apparent from the complete description provided hereinafter.
It should be understood that the complete description of exemplary embodiments is intended for illustration purposes only and is, therefore, not intended to necessarily limit the scope of the present disclosure.
DETAILED DESCRIPTION OF THE INVENTION
The present invention is more particularly described in the following present specification that is intended as illustrative only since numerous modifications and variations therein will be apparent to those skilled in the art. Various embodiments of the present disclosure are now described in detail. Referring to the drawings, like numbers, if any, indicate like components throughout the views. As used in the description herein and throughout the claims that follow, the meaning of "a", "an", and "the" includes plural reference unless the context clearly dictates otherwise. Also, as used in the description herein and throughout the claims that follow, the meaning of "in" includes "in" and "on" unless the context clearly dictates otherwise. Moreover, titles or subtitles may be used in the specification for the convenience of a reader, which shall have no influence on the scope of the present disclosure. Additionally, some terms used in this specification are more specifically defined below.
The terms used in this specification generally have their ordinary meanings in the art, within the context of the present disclosure, and in the specific context where each term is used. Certain terms that are used to describe the present disclosure are discussed below, or elsewhere in the specification, to provide additional guidance to the practitioner regarding the description of the disclosure.
For convenience, certain terms may be highlighted, for example using italics and/or quotation marks. The use of highlighting has no influence on the scope and meaning of a term; the scope and meaning of a term are the same, in the same context, whether or not it is highlighted. It will be appreciated that the same thing can be said in more than one way. Consequently, alternative language and synonyms may be used for any one or more of the terms discussed herein, nor is any special significance to be placed upon whether or not a term is elaborated or discussed herein. Synonyms for certain terms are provided. A recital of one or more synonyms does not exclude the use of other synonyms.
The use of examples anywhere in this specification including examples of any terms discussed herein is illustrative only, and in no way limits the scope and meaning of the disclosure or of any exemplified term. Likewise, the disclosure is not limited to various embodiments given in this specification.
Unless otherwise defined, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this disclosure pertains. In the case of conflict, the present document, including definitions will control.
As used herein, "around", "about" or "approximately" shall generally mean within 20 percent, preferably within 10 percent, and more preferably within 5 percent of a given value or range. Numerical quantities given herein are approximate, meaning that the term "around", "about" or "approximately" can be inferred if not expressly stated.
As used herein, "plurality" means two or more.
As used herein, the terms "comprising," "including," "carrying," "having," "containing," "involving," and the like are to be understood to be open-ended, i.e., to mean including but not limited to.
As used herein, the phrase at least one of A, B, and C should be construed to mean a logical (A or B or C), using a non-exclusive logical OR. It should be understood that one or more steps within a method may be executed in a different order (or concurrently) without altering the principles of the present disclosure.
Coconut Sprout Extract (CSE)
Coconut (Cocos nucifera) has been utilized for centuries in traditional medicine across various cultures, particularly in tropical regions. Its various parts, including the flesh, water, and oil, are known to possess a range of bioactive compounds that contribute to their therapeutic properties.
In particular, coconut sprouts, which emerge from the germinating coconut, have gained attention. The sprouting phase of the coconut has garnered attention due to its high concentration of bioactive compounds, including vitamins, minerals, and phytochemicals, which are hypothesized to contribute to various health benefits. Among these, the Coconut Sprout Extract (CSE) has shown potential in enhancing cognitive function and exhibiting neuroprotective properties.
The phytochemical profile of coconut sprouts includes antioxidants, flavonoids, and other bioactive compounds that have been shown to possess neuroprotective, anti-inflammatory, and antioxidant properties. The exploration of these properties has led to the investigation of coconut sprout extract (CSE) as a potential natural remedy for cognitive impairments associated with Alzheimer's disease.

Extraction of Coconut Sprout Extract (CSE)
An extraction process of CSE typically involves the use of solvents such as ethanol or water through methods like Soxhlet extraction, which enables the isolation of bioactive constituents while ensuring the preservation of their structural integrity. The resultant extract contains a complex mixture of phytochemicals, each contributing to the overall therapeutic efficacy of the formulation. Among these compounds, luteolin, saponins, phenolic acids, and ascorbic acid have been identified as key contributors to the neuroprotective effects of CSE.
The process begins with the selection of mature coconut sprouts, which are then cleaned and dried. The dried coconut sprouts are ground into a fine powder to increase the surface area for extraction. The powdered material is placed in a Soxhlet apparatus, where it is subjected to a solvent of choice. The extraction process may be monitored and controlled for specific parameters such as temperature, duration, and solvent type to optimize the yield of bioactive compounds.
Once the extraction is complete, the solvent is evaporated, and the remaining residue is the Coconut Sprout Extract (CSE), which may be standardized to contain specific active constituents known for their neuroprotective effects. This standardized extract may be then subjected to various analyses to evaluate its composition, efficacy, and safety profile.

Mechanism of Action of CSE in Alzheimer's Disease
The therapeutic potential of CSE in the context of Alzheimer's disease can be attributed to several interrelated mechanisms. Understanding these mechanisms is essential for elucidating how CSE exerts its beneficial effects on cognitive function and memory enhancement.
The therapeutic efficacy of CSE is attributed to its complex biochemical properties, which contribute to its potential in ameliorating Alzheimer's disease symptoms.
• Inhibition of Acetylcholinesterase (AChE): Alzheimer's disease is characterized by reduced levels of acetylcholine (ACh) due to cholinergic neuron degradation. CSE has shown the ability to inhibit AChE activity, leading to increased acetylcholine availability in the brain, which enhances memory and cognitive functions.
• Antioxidant Activity: CSE contains potent antioxidants, including ascorbic acid and various phenolic compounds, which counteract oxidative stress-a key factor in neurodegeneration. Additionally, CSE enhances the activity of antioxidant enzymes like catalase and glutathione peroxidase, further protecting neuronal cells from oxidative damage.
• Anti-inflammatory Properties: Neuroinflammation, driven by activated microglia and astrocytes, is a significant contributor to Alzheimer's pathology. CSE reduces inflammation by decreasing the levels of pro-inflammatory cytokines, thereby supporting neuronal health and function.
• Neuroprotective and Cognitive-Enhancing Effects: CSE contains bioactive phytochemicals such as luteolin and saponins, which promote neurogenesis, enhance neuronal plasticity, and protect against neuronal damage from oxidative and inflammatory stressors.
Experimental Design and Validation of Neuroprotective Effects
The neuroprotective and Cognitive-Enhancing effects of the present invention may be evaluated through a rigorously designed experimental study using Swiss albino mice. The evaluation may utilize 18 to 24-month-old adult Swiss albino mice (20-30 grams), of either sex, sourced from the central animal house at the Institute of Pharmaceutical Research, GLA University, Mathura. The choice of age group ensured that the subjects are mature adults, appropriate for modeling neurodegenerative conditions such as Alzheimer's disease.
Each group of test subjects may be housed in polypropylene cages with husk bedding in the institutional animal housing facility. The environmental conditions must be carefully controlled, with a temperature of 24±2°C, relative humidity of 45-55%, and a 12-hour light: 12-hour dark cycle. The mice are provided with regular pellet food (Lipton India, Ltd., Mumbai) and water ad libitum, ensuring a stable and stress-minimized environment throughout the experimental evaluation.
Further, all experimental procedures are conducted following the approval of the Institutional Animal Ethics Committee (IAEC/IPR-04/24-08GLAIPR), strictly adhering to the Committee for the Purpose of Control and Supervision of Experiments on Animals (CPCSEA) guidelines. Additionally, the protocols are aligned with the National Research Council's Guide for the Care and Use of Laboratory Animals (2011), to maintain the highest standards of animal welfare and ethical research practices.
Furthermore, the reagents used in this experimental evaluation of the present invention included scopolamine, trigonelline, and donepezil, sourced from Yarrow Pvt. Ltd., New Delhi. All chemicals used are of analytical grade to ensure consistency and accuracy in experimental outcomes.
Additionally, Coconut sprouts (Cocos nucifera L.) are obtained from a commercial source and authenticated at Botanical Garden and Institute of Research (BGIR), Noida, Uttar Pradesh, India. The raw plant material was subjected to identification and verification to confirm its botanical authenticity prior to extraction.
For the purpose of this evaluation, preferably but not limited to, 42 mice may be used, divided into seven distinct groups of six mice, with distinct treatment regimens as follows:
1. Group 1 - Control Group (CG)
Purpose: Baseline group to establish a reference for behavioral and biochemical comparisons.
Treatment: Distilled water (10 ml/kg, orally) once daily for 14 days. On the 7th day, 90 minutes post-administration, behavioral assessments were conducted.
2. Group 2 - Scopolamine Group
Purpose: Model group for Alzheimer's-like symptoms induced by scopolamine.
Treatment: Scopolamine (1 mg/kg, intraperitoneally) once daily for 7 days. On the 7th day, behavioral assessments were conducted 45 minutes post-treatment.
3. Group 3 - CSE 50 mg/kg Group
Purpose: To test the effects of a low dose of coconut sprout extract (CSE) on scopolamine-induced cognitive impairment.
Treatment: CSE (50 mg/kg, orally) once daily for 14 days, with scopolamine (1 mg/kg, i.p.) administered from the 7th to the 14th day, and behavioral assessments conducted thereafter.
4. Group 4 - CSE 100 mg/kg Group
Purpose: To assess the efficacy of a moderate dose of CSE in counteracting cognitive deficits.
Treatment: CSE (100 mg/kg, orally) once daily for 14 days, with scopolamine administered from the 7th to the 14th day, followed by behavioral testing.
5. Group 5 - CSE 150 mg/kg Group
Purpose: To examine a high dose of CSE for potential dose-dependent neuroprotective effects.
Treatment: CSE (150 mg/kg, orally) once daily for 14 days, with scopolamine administered on days 7-14, followed by behavioral testing.
6. Group 6 - CSE 100 mg/kg + Trigonelline Group
Purpose: To evaluate the synergistic effects of CSE combined with trigonelline.
Treatment: CSE (100 mg/kg, orally) and trigonelline (10 mg/kg, intraperitoneally) once daily for 14 days. Scopolamine was administered from the 7th to 14th day.
7. Group 7 - Donepezil (DPZ) Group
Purpose: Positive control to assess cognitive improvement against a standard Alzheimer's treatment.
Treatment: Donepezil (2.5 mg/kg, orally) once daily for 14 days, with scopolamine administered on days 7-14.
Behavioral Assessments: Morris Water Maze and Y-Maze Tests
To evaluate the cognitive-enhancing effects of CSE, a series of behavioral assessments may be conducted using established models for testing memory and learning capabilities in test subjects. The primary methodologies utilized ofr the purpose of present invention include the Morris Water Maze test and the Y-maze test. These assessments are designed to evaluate spatial learning, memory, and working memory in the test subjects/animals, providing a robust measure of cognitive function.
1. Morris Water Maze Test (MWM): The Morris Water Maze test is a widely used behavioral assay to evaluate spatial learning and memory in rodents. In this test, animals are placed in a circular pool filled with opaque water, where a submerged platform is hidden just below the surface. The time taken by the animal to locate the platform and the distance traveled to reach it are measured. A decrease in latency to find the platform indicates improved spatial learning and memory retention. The results demonstrated that the CSE-treated mice showed a marked reduction in the time taken to locate the platform compared to the scopolamine-treated group, further supporting the cognitive-enhancing properties of CSE.
FIG. 3 (A) discloses effect of CSE on Escape latency by using Morris Water Maze. It shows that when scopolamine is administered, it significantly increases the escape latency value of (55.55±1.59) compared to the normal group (15.16±0.36). However, when donepezil is given, it significantly decreased the escape latency value (25±0.81) compared to the scopolamine-treated group. Similarly, administration of CSE at the doses of 50mg/kg, 100mg/kg, 150mg/kg results in a significant decrease in escape latency value (for 50mg/kg 35.33±1.08, for 100mg/kg 30±0.81, 150mg/kg 40±1.08) compared to the scopolamine treated group. However, all groups treated with CSE 50mg/kg, 100mg/kg, 150mg/kg showed decreased time to escape onto the escape platform and trigonelline reduced the effect of CSE 100mg/kg, to with significant values (P<0.0001). This proves that trigonelline act as a blocker which interfere with the effect of our test drug. The pathway which involved in it mechanism may be the Nrf2 which can be further studied and proved by various techniques.
Further, all values in the figure are mean ± SEM (n=6). ap<0.05 compared to control, bp<0.05 compared to scopolamine, cp<0.05 compared to scop + CSE50mg/kg, dp<0.05 compared to scopolamine + CSE100mg/kg, ep<0.05 compared to scop + TGN+CSE100 mg/kg, fp<0.05 compared to donepezil.
2. Y-Maze Test: The Y-maze test assesses spatial memory and cognitive flexibility in rodents. The maze consists of three arms, and animals are allowed to explore the maze freely. The percentage of alternation behavior, which is defined as the number of times an animal visits all three arms in a consecutive sequence, is measured. An increase in alternation behavior indicates enhanced working memory. The CSE-treated group exhibited a statistically significant increase in alternation behavior compared to the control group, suggesting improved cognitive function.
FIG. 3 (B) discloses treatment effect of CSE on Percentage alteration by using Y Maze. It shows that administration of scopolamine resulted in a significant (P<0.001) decreased percentage alteration value (35.16±3.3) as compared to the normal group (65.35±2.6). Administration of at the dose of 2.5mg/kg, has resulted in significant increased percentage alteration value (54.8±2.1) as compared to the scopolamine group. It is observed that administration of CSE resulted in a significant (P<0.001) increased percentage alteration value (50mg/kg 45.83±6.3, for 100mg/kg 53.5±2.5 and for 150mg/kg 50.3±3.5) as compared to the scopolamine treated group. The Alzheimer's induced group (negative control) indicated decrease in the alternation of behavior. The results presented by the treatment groups showed significance by (P<0.001) increase in alteration of behavior in respect of 50mg/kg of CSE, 100mg/kg, 150mg/kg of CSE when compared with that of the disease control group. Trigonelline reduced the effect of CSE 100mg/kg, to with significant values (P<0.0001). This proves that trigonelline act as a blocker which interfere with the effect of the test drug. The pathway which involved in it mechanism may be the Nrf2 which can be further studied and proved by various techniques.
Further, all the values in the figure are mean ± SEM (n=6). ap<0.05 compared to control, bp<0.05 compared to scopolamine, cp<0.05 compared to scop + CSE50mg/kg, dp<0.05 compared to scopolamine + CSE100mg/kg, ep<0.05 compared to scop + TGN+CSE100 mg/kg, fp<0.05 compared to donepezil.

Biochemical Analysis
After the behavioral assessments, biochemical analyses may be performed on the brain tissues of the experimental groups to elucidate the mechanisms underlying the observed cognitive improvements. Key parameters that may be evaluated, but not limited to, include acetylcholinesterase (AChE) activity, levels of reduced glutathione (GSH), malondialdehyde (MDA) levels, and catalase activity.
• AChE Activity: The determination of AChE activity in the brain tissue is critical for assessing the cholinergic effects of CSE. A significant reduction in AChE activity was observed in the CSE-treated group compared to the scopolamine group, indicating that CSE effectively inhibits the breakdown of acetylcholine, thereby enhancing cholinergic transmission.
FIG. 4 discloses CSE decreases acetylcholinesterase level in scopolamine induced Alzheimer's in subjects. The figure assesses the level of AChE in the whole brain homogenate of all groups to evaluate the anti-Alzheimer's activity. Administration of scopolamine resulted in a significant increase in AChE values (2.4±0.10) compared to the normal group (2.34±0.04). However, when given, it significantly decreased AChE values (1.2±0.05) compared to the scopolamine treated group. Similarly, administration of CSE at the doses of 50mg/kg, 100mg/kg and 150mg/kg resulted in a significant decrease in AChE values (for 50mg/kg 1.78±0.02), for 100mg/kg (1.4±0.04) and for 150mg/kg (1.6±0.01) compared to the scopolamine treated group.
Both and CSE demonstrated significant anti-Alzheimer's activity, and CSE showed a synergistic effect with in treating scopolamine - induced Alzheimer's in mice. There was an increase in AChE activity in the disease control group compared to the control group, with a significant difference (p<0.0001). These findings indicate that CSE may have a beneficial effect in improving memory and cognitive function by modulating AChE activity in the brain. Trigonelline reduced the effect of CSE 100mg/kg, to with significant values (P<0.001). This proves that trigonelline act as a blocker which interfere with the effect of the test drug. The pathway which involved in it mechanism may be the Nrf2 which can be further studied and proved by various techniques.
Further, all values in the figure are mean ± SEM (n=6). ap<0.05 compared to control, bp<0.05 compared to scopolamine, cp<0.05 compared to scop + CSE50mg/kg, dp<0.05 compared to scopolamine + CSE100mg/kg, ep<0.05 compared to scop + TGN+CSE100 mg/kg, fp<0.05 compared to donepezil.
• Catalase Activity: Catalase is an enzyme that catalyzes the decomposition of hydrogen peroxide into water and oxygen, playing a crucial role in cellular antioxidant defenses. The increase in catalase activity in the CSE-treated group further supports the antioxidant capacity of CSE, highlighting its potential in protecting neuronal cells from oxidative stress.
FIG. 5 discloses CSE increased Catalase level in scopolamine induced Alzheimer's in subjects. The study aimed to determine the level of catalase in the whole brain homogenate of all animal groups to assess the anti-Alzheimer's activity. Administration of scopolamine resulted in a significant decrease in catalase values (9.75±0.05) compared to the normal group (29.3±0.3). However, when was given, it significantly increased the catalase value (24.73±0.2) compared to the scopolamine-treated group. On the other hand, administration of CSE at the doses of 50mg/kg, 100mg/kg, 150mg/kg resulted in a significant decrease in catalase values (for 50mg/kg (25.02±0.12), for 100mg/kg (35.2±0.8)) compared to the scopolamine-treated group. CSE displayed a synergistic effect within treating scopolamine-induced amnesia in mice. There was an increase in catalase level in the disease control group compared to the control group, with a significant difference (p<0.001).
These findings suggest that CSE, similar to, may influence catalase levels in the brain,
contributing to its memory enhancing effects and potential therapeutic role in Alzheimer's. Trigonelline reduced the effect of CSE 100mg/kg, to with significant values (P<0.0001). This proves that trigonelline act as a blocker which interfere with the effect of our test drug. The pathway which involved in it mechanism may be the Nrf2 which can be further studied and proved by various techniques.
Further, all values in the figure are mean ± SEM (n=6). ap<0.05 compared to control, bp<0.05 compared to scopolamine, cp<0.05 compared to scop + CSE50mg/kg, dp<0.05 compared to scopolamine + CSE100mg/kg, ep<0.05 compared to scop + TGN+CSE100 mg/kg, fp<0.05 compared to donepezil.
• Levels of Reduced Glutathione (GSH): GSH is a vital antioxidant that protects cells from oxidative damage. The CSE treatment significantly elevated GSH levels in the brain tissue, demonstrating its capacity to enhance the brain's antioxidant defense system. This elevation is crucial for countering oxidative stress associated with Alzheimer's disease.
FIG. 6 discloses CSE increased level of GSH in scopolamine induced Alzheimer's in subjects. The study evaluated the level of glutathione reductase in the whole brain homogenate of all animal groups to assess the anti-Alzheimer's activity. Administration of scopolamine resulted in a significant decrease in glutathione reductase values (1.5±0.05) compared to the normal group (4.26±0.3). However, when was given, it significantly increased the glutathione reductase value (2.83±0.2) compared to the scopolamine-treated group. On the other hand, administration of CSE at the doses of 50mg/kg, 100mg/kg, 150mg/kg resulted in a significant decrease in glutathione reductase values for 50mg/kg (1.86±0.12), for 100mg/kg (2.4±0.8) compared to the scopolamine-treated group. Both and CSE showed significant Anti-Alzheimer's activity, and CSE displayed a synergistic effect with in treating scopolamine-induced amnesia in mice. There was an increase in glutathione reductase level in the disease control group compared to the control group, with a significant difference (p<0.001). These findings suggest that CSE, similar to , may influence glutathione reductase levels in the brain, contributing to its memory enhancing effects and potential therapeutic role in Alzheimer's. Trigonelline reduced the effect of CSE 100mg/kg, to with significant values (P<0.0001). This proves that trigonelline act as a blocker which interfere with the effect of our test drug. The
pathway which involved in it mechanism may be the Nrf2 which can be further studied and proved by various techniques.
Further, all values in the figure are mean ± SEM (n=6). ap<0.05 compared to control, bp<0.05 compared to scopolamine, cp<0.05 compared to scop + CSE50mg/kg, dp<0.05 compared to scopolamine + CSE100mg/kg, ep<0.05 compared to scop + TGN+CSE100 mg/kg, fp<0.05 compared to donepezil.
• Malondialdehyde (MDA) Levels: MDA is a marker of lipid peroxidation and oxidative stress. The levels of MDA were significantly lower in the CSE-treated group compared to the control group, indicating that CSE helps to mitigate lipid peroxidation and protect neuronal integrity from oxidative damage.
FIG. 7 discloses CSE decreased MDA level in scopolamine induced Alzheimer's in subjects. The study aimed to determine the level of MDA in the whole brain homogenate of all animal groups to assess the nootropic activity. Administration of scopolamine resulted in a significant increase in MDA values (106.31±2.33) compared to the normal group (62.838±3.23). However, when was given, it significantly increased the MDA value (60.52±0.2) compared to the scopolamine-treated group. On the other hand, administration of CSE at the doses of 50mg/k,100mg/kg,150mg/kg resulted in a significant increase in catalase values for 50mg/kg (76.89±3.12), for 100mg/kg (68.36±5.8) and for 150 mg/kg (93.25±2.2) compared to the scopolamine-treated group. Both and CSE showed significant activity, and CSE displayed a synergistic effect with in treating scopolamine-induced amnesia in mice. There was an increase in MDA level in the disease control group compared to the control group, with a significant difference (p<0.001) as shown in the figure. Trigonelline reduced the effect of CSE 100mg/kg, to with significant values (P<0.0001). This proves that trigonelline act as a blocker which interfere with the effect of our test drug. The pathway which involved in it mechanism may be the Nrf2 which can be further studied and proved by various techniques.
Further, all values in the figure are mean ± SEM (n=6). ap<0.05 compared to control, bp<0.05 compared to scopolamine, cp<0.05 compared to scop + CSE50mg/kg, dp<0.05 compared to scopolamine + CSE100mg/kg, ep<0.05 compared to scop + TGN+CSE100 mg/kg, fp<0.05 compared to donepezil.
The embodiments described hereinabove are exemplary of the present invention. The disclosure may enable those skilled in the art to make and use embodiments having alternative elements that likewise correspond to the elements of the invention. The intended scope of the invention may thus include other embodiments that do not differ or that insubstantially differ from the literal language of the invention. However, the scope of the present invention is accordingly defined as set forth in the present complete specification.
, Claims:We Claim;
1. A pharmaceutical composition for enhancing cognitive function, comprising:
coconut sprout extract (CSE) in a concentration of 50 mg/kg to 150 mg/kg,
an additional therapeutic agent selected from the group consisting of trigonelline and donepezil, and
a pharmaceutically acceptable carrier.

2. The pharmaceutical composition as claimed in Claim 1, wherein the coconut sprout extract is present in a concentration of 100 mg/kg.

3. The pharmaceutical composition as claimed in Claim 1, wherein the additional therapeutic agent is trigonelline in a concentration of 10 mg/kg.

4. The pharmaceutical composition as claimed in Claim 1, wherein the additional therapeutic agent is donepezil in a concentration of 2.5 mg/kg.

5. The pharmaceutical composition as claimed in Claim 1, wherein the composition further comprises an antioxidant compound selected from ascorbic acid, squalene, or a pharmaceutically acceptable salt thereof.

6. The pharmaceutical composition as claimed in Claim 1, wherein the pharmaceutically acceptable carrier is selected from water, saline, or a buffered solution.

7. The pharmaceutical composition as claimed in Claim 1, wherein the composition is formulated for oral administration.

8. The pharmaceutical composition as claimed in Claim 1, wherein the coconut sprout extract is combined with an emulsifying agent selected from lecithin or glycerol monostearate to enhance bioavailability.

9. The pharmaceutical composition as claimed in Claim 1, wherein the composition additionally comprises a preservative selected from sodium benzoate or potassium sorbate to improve stability during storage.

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