INTRODUCTION:

1.1 What is Alzheimer’s Disease?

Alzheimer’s disease is a chronic neurodegenerative disease that destroys brain cells, causing a decline in thinking ability and memory over time. Alzheimer’s disease is not a normal part of aging and is irreversible.

AD is named after the German physician Alois Alzheimer. He described the symptoms of a patient known as “Auguste D.” In 1906. The symptoms were:

1) Memory loss

2) Abnormal behavior

3) Shrinking of the patient’s brain

Psychiatrist Emil Kraepelin, a colleague of Dr. Alzheimer’s disease, coined the name “Alzheimer- disease” in a 1910 medical book.¹

In 1901, Alois Alzheimer, a young psychiatrist in his 30s, met Auguste Deter, marking the beginning of a significant chapter in medical history. Dr. Alzheimer, who was deeply committed to exploring the connections between brain diseases and mental illnesses, was working at the Community Hospital for Mental and Epileptic Patients in Frankfurt, Germany. Following the death of his wife earlier that year, he immersed himself in his clinical duties.

Auguste Deter, later known as “Auguste D,” was 50 years old when her husband noticed her worsening memory problems. Her condition rapidly progressed, leading to increased fearfulness, paranoia, and aggression. By age 51, these symptoms necessitated her admission to the psychiatric hospital where she remained until her death in 1906. By the time of her death, Dr. Alzheimer had moved to a research position at the Munich Hospital under Dr. Emil Kraepelin, a prominent psychiatrist of that era. Dr. Emil Sioli, Alzheimer’s former superior in Frankfurt, informed him of Deter’s death and sent her brain material for further examination. Using innovative staining techniques, Alzheimer discovered what we now identify as amyloid plaques and neurofibrillary tangles in her brain. Despite the groundbreaking nature of his findings, Alzheimer’s initial 1906 presentation linking specific brain pathology to a clinical syndrome received a lukewarm reception from his contemporaries.²

Symptoms:

The symptoms appear gradually, over months or years. If they develop over hours or days, a person may require medical attention, as this could indicate a stroke.

Symptoms of Alzheimer’s Disease Include:

· Memory loss: A person may have difficulty taking in new information and remembering information. This can lead to:

a. Repeating questions or conversations

b. Losing objects

c. Forgetting about events or appointments

d. Wandering or getting lost

· Cognitive deficits: A person may experience difficulty with reasoning, complex tasks, and judgment.

This can lead to:

a. A reduced understanding of safety and risks

b. Difficulty with money or paying bills

c. Difficulty making decisions

d. Difficulty completing tasks that have several stages, such as getting dressed

· Problems with recognition: A person may become less able to recognize faces or objects or less able to use basic tools. These issues are not due to problems with eyesight.

· Problems with spatial awareness: A person may have difficulty with their balance, trip over, or spill things more often, or they may have difficulty orienting clothing to their body when getting dressed.

· Problems with speaking, reading, or writing: A person may develop difficulties with thinking of common words, or they may make more speech, spelling, or writing errors.

· Personality or behaviour changes: A person may experience changes in personality and behaviour that include:

a. Becoming upset, angry, or worried more often than before

b. A loss of interest in or motivation for activities they usually enjoy

c. A loss of empathy

d. Compulsive, obsessive, or socially inappropriate behaviour³

Pathophysiology:

Alzheimer’s disease is characterized by the accumulation of abnormal neural plaques and neurofibrillary tangles. Plaques are spherical microscopic lesions with a core of extracellular amyloid-beta peptide surrounded by enlarged axon terminals. Beta-amyloidpeptide originates from a transmembrane protein known as amyloid precursor protein (APP). Beta-amyloid peptide is cleaved from APP by proteases called alpha-, beta-, and gamma-secretase. Generally, APP is cleaved by either alpha- or beta-secretase, and the resulting small fragments are not toxic to neurons. However, sequential cleavage by beta and then gamma-secretase results in a 42 amino acid peptide (beta-amyloid 42). Increased levels of beta-amyloid 42 cause amyloid aggregation, which leads to neurotoxicity. Beta amyloid 42 promotes the formation of aggregated fibrillary amyloid protein instead of the normal degradation of APP. The APP gene is located on chromosome 21, one of the regions associated with familial Alzheimer’s disease. In Alzheimer’s disease, amyloid deposits occur around the meninges and cerebral blood vessels, as well as gray matter. Gray matter is multifocal and coalesces to form miliary structures called plaques. But brain scans found amyloid plaques in some people with dementia and then others who had dementia but brain scans found no plaque. ⁴Neurofibrillary tangles are filamentous intracytoplasmic structures in neurons formed by a protein called tau. The primary function of the tau protein is to stabilize axon microtubules. Microtubules run along the axons of neurons and are essential for intracellular transport. The assembly of microtubules is held together by the tau protein. In Alzheimer’s disease, hyperphosphorylation of tau occurs due to aggregation of extracellular beta-amyloid, which then leads to the formation of tau aggregates. Tau aggregates form twisted helical filaments called neurofibrillary tangles They first appear in the hippocampus and then are seen throughout the cortex. Tau aggregates are deposited in neurons. There is a staging system developed by Braak and Braak based on the topographic staging of neurofibrillary tangles in 6 stages, and this Braak staging is an integral part of the National Institute on Aging and the Reagan Institute neuropathological criteria for the diagnosis of Alzheimer’s disease. Tangles correlate more strongly with Alzheimer’s disease than plaques, another hallmark of Alzheimer’s disease is the granulovacuolar degeneration of hippocampal pyramidal cells caused by amyloid angiopathy. Some reports indicate that cognitive decline correlates with a decrease in the density of presynaptic neurons in laminae III and IV pyramidal neurons rather than an increase in the number of spikes. Loss of the nucleus of the nucleus of Myenert, leading to low levels of acetylcholine, has also been observed. Weighed.⁵

Figure 1: Pathophysiology of Alzheimer’s Disease

The role of blood vessels in the neurodegenerative process of Alzheimer’s disease is not fully established. In connection with subcortical infarcts, the risk of dementia increases fourfold. Cerebrovascular disease also increases the level and incidence of dementia. ^[6]

Plant Profile:

General Information:

Common name - Green Amaranth, pigweed, Prince of Wales feather, slender amaranth, Tropical green amaranth

Synonym- Amaranthus gracilis, Amaranthus polystachyus, Euxolus viridis

Family – Amaranthaceae – Amaranth family⁷

a) Whole Plant b) Leaves:

Figure 2: Amaranthus viridis Linn. Plant

Botanical Discription:

Amaranthus viridis L. is an annual herb with an upright, light green stem that grows to about 60-80Cm in height. Numerous branches emerge from the base, and the leaves are ovate, 3-6cm Long and 2-4cm wide, long petioles of about 5cm. The plant has terminal panicles with few Branches, and small green flowers.

Ecology:

Amaranthus viridis L. thrives in well-drained soil and requires a sunny location. It should not be given inorganic fertilizers. The plant is cultivated as a food source in tropical regions and uses the C4 carbon fixation pathway, which is efficient at high temperatures.⁸

Propogation:

Amaranthus viridis L. is propagated by sowing seeds in spring. Germination is rapid if the soil is warm. A drop in temperature overnight will assist the germination. Apart from seeds the cuttings of growing plants are also used for propagation which roots easily.⁹

Phytochemistry:

Amaranthus viridis L. Shows the range of chemical constituents that contribute to its Medicinal value leaves and seeds are rich in components valuable according to the medicinal Point of view. Leaves of Amaranthus viridis L. Contain reducing sugar, resin, tannin , cardiac glycosides, Phlobatannins, flavonoids zinc, protein, calcium, alpha-linoleic acid, linoleic acid, iron, magnesium and Beta-carotene. Roots of the Amaranthus viridis L. contain Amasterol. Seeds of Amaranthus viridis L. contain Triacontane, Saponins, Ecdysteron, Pentatriacontane, Hentriacontane, Hexatriacontane, 6-Pentatriacontane, and Cardiac glycosides. Barren palatable plants contain Oxalic acid and carotenoids.¹⁰

MATERIAL AND METHOD:

Experimental Animals:

8 weeks old healthy female Sprague-Dawley rats (weighing 150-250gm) were used for this study. Animals were housed in polypropylene cages with wire mesh top and husk bedding and maintain under control condition of light (12h-light, 12h-dark), temperature (25±2ºC), and humidity (60±5%) and fed with a standard pellet diet and water. The experiments were performed during day (8.00-16.00hrs). The rats were housed and treated according to the rules and regulations of CPCSEA and IAEC. The protocol for all the animal study was approved by Institutional Animal Ethics Committee. (IAEC) with the research project number 650/PO/Re/ 8-2002/2024/ CCSEA/10.

Apparatus and Instruments:

Weighing balance, Magnetic stirrer, Cooling centrifuge, Tissue homogenizer, Morris Water maze apparatus, plus maze apparatus

Chemicals and Reagents:

Methanol, Molisch reagent, Mayers reagent, Sulfuric acid, Lead acetate, Ferric chloride, Sodium hydroxide, Anesthetic Ether, Scopolamine, Acetylthiocholine, DTNB.

Methods:

Collection, Identification and Authentication of Plant Material:

The plant of Amaranthus viridis Linn. was collected in the month of January, 2023 from Murtizapur, Akola district, Maharashtra, India. The plant material was identified and authenticated by Mrs. A. M. Gaharwar, Assistant Professor of Vasantrao Naik College of Agricultural Biotechnology, Yavatmal. (Reference no. VNCABT/Ytl/Hort/1901/2024CCS

Shade drying and Granulation:

The plant leaves were taken and dried in shade. Then the shade-dried leaves were coarsely powdered by means of a mixer grinder and passed through sieve no. 60 to get the coarse powder. Then the coarsely powdered materials were weighed, packed in an airtight container, and used for extraction with solvent, phytochemical studies, and pharmacological studies.

Preparation of plant extract:

About 350gm of coarsely powdered leaves were packed in 1000ml Soxhlet apparatus and extracted with methanol for 72 hours by continuous hot percolation. After extraction, the solvent was distilled off and extract was concentrated at room temperature and the percentage yield was calculated.

Experimental Design:

Rats were divided in five groups (n=6) for this study.

Group I (Vehicle Control):

Rats were treated with normal saline solution.

Group II (Negative Control):

Rats were treated with scopolamine (2mg/kg,i.p.) for 21 days.

Group III (Low Dose):

AD induced rats were treated with Amaranthus viridis L. extract (200mg/kg,p.o.) for 21 days.

Group IV (High Dose):

AD induced rats were treated with Amaranthus viridis L. (400mg/kg,p.o.) extract for 21 days.

Group V (Standard):

AD induced rats were treated with Donepezil drug (5mg/kg,p.o.) for 21 days

Evaluation of learning and memory impairment in Rats after inducing AD:

All animals in each group were assessed for the learning and memory impairment state by following animal models.

1. Elevated plus maze apparatus.

2. Morris water maze apparatus.

Readings of all animals in each group were noted down. These readings were referred as a 0 day before inducing Alzheimer’s disease. These reading were compared with the Readings of animal models after inducing Alzheimer’s disease i.e., after 21 days.

Induction of Alzheimer’s disease by using scopolamine:

Alzheimer’s disease and associated memory impairment was induced in rats using muscarinic acetylcholine receptor (M1) blocking agents i.e. Scopolamine (2mg/kg i.p.).

Daily Dosing of Amaranthus viridis L. Leaves Extract:

Daily dose was given to group III and IV MEAV 200mg/kg and MEAV 400mg/kg respectively. Daily dose of extract was given for the duration of 21 days.

Statistical Analysis:

Results were expressed as Mean±SD for statistical analysis of the data. Group means were compared by one way ANOVA followed by Dunnet’s test. The data was statistically analyzed by using Graphpad instat Software. P<0.01 was considered to be statistically significant.

Biochemical Estimation:

Brain Acetylcholinesterase Activity

Methodology

Reagents

1. 0.1 M Phosphate buffer:

· Solution A: 5.22g of K2HPO4 and 4.68g of NaH, PO, were dissolved in 150 ml of distilled water.

· Solution B: 6.2g NaOH was dissolved in 150ml of distilled water.

· Solution B was added to solution A to get the desired pH (pH 8.0 or 7.0) and then finally the volume is made up to 300ml with distilled water.

2. DTNB Reagent:

· 39.6mg of DTNB with 15mg NaHCO3, was Dissolved in 10ml of 0.1M phosphate buffer (pH 7.0).

3. Acetylthiocholine (ATC)

· 21.67mg of acetylthiocholine was dissolved in 1ml of distilled water.

Assay Procedure:

1. Dissection rats (250-300g body weight) were used for the experiment. The rats were decapitated; brains were removed quickly and placed in ice-cold saline. Frontal cortex, hippocampus and septum (and any other regions of interest) are quickly dissected out on a petri dish chilled on crushed ice.

2. The tissues were weighed and homogenized in 0.1M Phosphate buffer (pH 8).

3. 0.4ml aliquot of the homogenate was added to a cuvette containing 2.6 ml phosphate buffer (0.1M, pH 8) and 100µl of DTNB.

4. The contents of the cuvette were mixed thoroughly by bubbling air and absorbance is measured at 412 nm in a LKB spectrophotometer. When absorbance reaches a stable value, it was recorded as the basal reading.

5. 20µl of substrate i.e., acetylthiocholine was added and change in absorbance wasrecorded for a period of 10 mins at intervals of 2 mins. Change in the absorbance per minute was thus determined.

Calculations:

The enzyme activity is calculated using the following formula;

R=5.74 x 10-4 x A/CO

Where,

R= Rate in moles of substrate hydrolyzed / minute/gm tissue

A = Change in absorbance/min

CO = Original concentration of the tissue (mg/ml).11

RESULTS:

Elevated Plus Maze Apparatus

Table No. 1: Effect of MEAV on Transfer Latency on day 0 and day 21 in rats

Sr. No.	Groups	Transfer Latency on day 0 (sec)	Transfer Latency on day 21 (sec)
1.	Normal Control	44.66± 5.39	46.16±11.28
2.	Negative Control	38.66±11.91	80.5±8.87^@
3.	MEAV (200mg/kg)	37.66±3.72	53.16±7.83**
4.	MEAV (400mg/kg)	54.66±4.92	40.83±5.70**

Figure No. 3: Effect of MEAV on Transfer Latency on day 0 and day 21 in rats

All values are Mean±SD @ p<0.01 Significant increase in transfer latency was observed compared to normal control group. **p<0.01 significant decrease in transfer latency was observed compared to negative control group.

Table 1 and Figure 3 shows the effect of Amaranthus viridis L. extract on transfer latency (TL) on day 0 and day 21 in rats. There was significant (p<0.01) increase in TL in negative control group as compare to normal control group. There was significant (p<0.01) decrease in TL in MEAV 200mg/kg, MEAV 400mg/kg and donepezil treated group when compared to negative control group on day 21.

Morris Water Maze Apparatus:

Table No. 2: Effect of MEAV on Escape Latency on day 0 and day 21 in rats

Sr. No.	Groups	Escape Latency on day 0 (sec)	Escape Latency on day 21 (sec)
1.	Normal Control	11.49±0.96	10.66±1.36
2.	Negative Control	11.49±1.89	17.72±1.66^@
3.	MEAV (200mg/kg)	12.10±0.75	12.24±2.72**
4.	MEAV (400mg/kg)	13.44±2.72	12.10±2.09**
5.	Donepezil (5mg/kg)	11.49±1.28	10.92±1.17**

Figure No. 4: Effect of MEAV on escape latency on day 0 and day 21 in rats

All values are Mean±SD @p<0.01 significant increase in escape latency was observed compared with normal control group, **p<0.01 significant decrease in escape latency was observed compared with negative control group.

Table 2 and figure 4 shows the effect of Amaranthus viridis L. leaves extract on escape latency on day 0 and day 21 in rats. There was significant (P<0.01) increase in escape latency in negative control group as compare to the normal control group. There was significant (P<0.01) decrease in escape latency in MEAV 200mg/kg, MEAV 400mg/kg and donepezil treated group when compared to negative control group on day 21.

Table No. 3: Effect of MEAV on Retention Time on day 0 and day 21 in rats

Sr. No.	Groups	Retention Time on day 0 (sec)	Retention Time on day 21 (sec)
1.	Normal Control	73.33±4.59	75.66±3.61
2.	Negative Control	68.33±9.56	30.33±4.03@
3.	MEAV (200mg/kg)	70.33±6.59	44.33±4.03**
4.	MEAV (400mg/kg)	78.66±3.14	58.5±3.98**
5.	Donepezil (5mg/kg)	78±4.98	76.33±5.75**

Figure No.5: Effect of MEAV on Retention Time on day 0 and day 21 in rats.

All values are Mean±SD @p<0.01 significant decrease in retention time was observed compared with normal control group, **p<0.01 significant increase in escape latency was observed compared with negative control group.

Table 3 and figure 5 shows the effect of Amaranthus viridis L. leaves extract on retention time on day 0 and day 21 in rats. There was significant (P<0.01) decrease in retention time in negative control group as compared to the normal control group. There was significant (P<0.01) increase in retention time in MEAV 200mg/kg, MEAV 400mg/kg and donepezil treated group when compared to negative control group on day 21.

Estimation of Biochemical Parameter:

Brain Acetyl Cholinesterase (AChE) Activity in rats:

Table No. 4: Effect of MEAV on brain AChE activity on day 21 in rats

Sr. No.	Groups	Brain AchE activity in rats (µ moles/min/gmtissue)
1.	Normal Control	3.44±0.25
2.	Negative Control	12.05±0.25@
3.	MEAV (200mg/kg)	9.15±0.22**
4.	MEAV (400mg/kg)	6.31±0.25**
5.	Donepezil (5mg/kg)	4.58±0.25**

Figure No. 6: Effect of MEAV brain AChE activity on day 21 in rats

All values are Mean±SD @p<0.001 significant increase in brain AchE activity was observed compared with normal control group, **p<0.01 significant decrease in brain AchE activity was observed compared with negative control group. nsP>0.05 when compared with negative control group.

Table 4 and figure 6 shows the effect of Amaranthus viridis L. on brain AChE activity on day 21 in rats. There was significant (P<0.01) increase in the AChE activity in negative control group as compared to the normal control group. There was significant (P<0.01) decrease in AChE activity in MEAV 200mg/kg, MEAV 400mg/kg and donepezil treated group when compared to negative control group on day 21.

DISCUSSION:

The methanolic extract of leaves of Amaranthus viridis Linn. was evaluated for its Antialzheimer’s activity. Preliminary phytochemical analysis revealed the presence of alkaloids, carbohydrates, saponins, glycosides, protein and amino acids, phenolic compounds in the methanolic extract. This study aimed to evaluate the anti-Alzheimer's activity of Amaranthus viridis Linn extract using rat models assessed through the Morris Water Maze (MWM) and Elevated Plus Maze (EPM). Alzheimer's disease was induced in rats via a neurotoxin scopolamine

The plant extract was prepared by drying, powdering, and extracting Amaranthus viridis Linn leaves with methanol. Rats were divided into Normal control, Negative control, MEAV 200mg/kg, MEAV 400mg/kg and donepezil group and received treatment as per schedule for 21 days. In the MWM test, which measures spatial learning and memory, rats treated with the MEAV 200mg/kg, MEAV 400mg/kg and donepezil showed a significant reduction in escape latency compared to the Negative control group, indicating improved cognitive function. Retention time in the context of the Morris Water Maze (MWM) refers to the duration the rats remember the location of the hidden platform during the probe trial, where the platform is removed, and the rats are expected to swim in the area where the platform was previously located. Higher retention time indicates better memory retention and spatial learning. Rats treated with MEAV 200 mg/kg, MEAV 400mg/kg and donepezil demonstrated significantly higher retention times compared to the negative control group, indicating enhanced memory retention and cognitive function. This improvement suggests that the extract positively affects the neural mechanisms involved in memory and learning, likely due to its neuro protective properties. In EPM test, the results likely showed a decrease in transfer latency in rats treated with the MEAV 200mg/kg, MEAV 400 mg/kg and donepezil when compared to negative control group. The assessment of biochemical parameter, Brain acetylthiocholine activity, provides mechanistic insights into the mode of action of the Amaranthus viridis Linn extract. Acetylcholine is a neurotransmitter involved in various cognitive functions, and its depletion is a hallmark of AD. The observed increase in brain acetylthiocholine activity following treatment with the MEAV 200mg/kg, MEAV 400mg/kg extract indicates its potential to enhance cholinergic neurotransmission, which is beneficial for memory and cognitive processes. This suggests that the Amaranthus viridis Linn extract may exert its anti-Alzheimer’s effects, at least in part, through modulation of cholinergic signaling pathways.

This result, combined with the biochemical findings, supports the potential of Amaranthus viridis Linn extract as a promising therapeutic agent for mitigating symptoms of Alzheimer’s disease. These findings support further investigation into the specific neuroprotective mechanisms underlying its effects and its potential as a novel therapeutic agent for the treatment of Alzheimer’s disease. Further research is warranted to elucidate the optimal dosage, treatment duration, and long-term effects of the extract, as well as its potential synergistic interactions with existing pharmacotherapies for AD.

CONCLUSION:

The pharmacological evaluation of Amaranthus viridis Linn plant extract for its anti-Alzheimer’s activity presents promising findings indicative of its potential therapeutic efficacy. Through a combination of behavioral assessments using rat models like the Morris Water Maze and Elevated Plus Maze, along with biochemical analyses focusing on parameters such as brain acetylcholine activity, the study provides compelling evidence of the extract’s neuroprotective and cognitive-enhancing properties. Results demonstrate significant improvements in spatial learning, memory retention, and reduced anxiety-like behavior in rats treated with the MEAV 200 mg/kg, MEAV 400 mg/kg extract and donepezil when compared to negative control group. Moreover, the observed increase in brain acetylcholine activity suggests that the extract may modulate cholinergic neurotransmission, a critical pathway implicated in Alzheimer’s pathology. These findings underscore the potential of Amaranthus viridis Linn extract as a novel therapeutic agent for Alzheimer’s disease, warranting further investigation into its specific mechanisms of action and clinical translation.

Overall, this study contributes valuable insights into the search for alternative treatments for Alzheimer’s disease and highlights the importance of exploring natural compounds with neuroprotective properties in combating this debilitating condition.

FUTURE PROSPECTIVES:

The current study reveals that methanolic extract of Amaranthus viridis L. is having Antialzheimer’s activity, So in future we can go for,

1. A lead molecule having the Anti-alzheimer’s activity which can be isolated from the extract of plant Amaranthus viridis L.

2. Amaranthus viridis L. is an interesting weed vegetable with a good nutritional value.

3. It certainly deserves more attention to determine wider domestication possibilities and optimum cultivation practices.

4. Its medicinal properties need further investigation as well.

5. More research is needed into the nutritional aspects and utilization of the Amaranthus Viridis L. in the treatment of AD.

REFERENCES:

1. Timothy J. Legg, A Brief History of Alzheimer’s Disease. National Library of Medicine. 2017; 1(5): 55-57.

2. James M. Ellison, The History of Alzheimer’s Disease. Sci. Transl. Med. 2021; 17(2): 34-38.

3. Seunggu Han, M.D, Markus Mac Gill What to know about Alzheimer’s disease. Healthline. 2023; 34(2): 120-122.

4. Verma M, Wills Z, Chu CT. Excitatory Dendritic Mitochondrial Calcium Toxicity: Implications for Parkinson's and Other Neurodegenerative Diseases. Front Neurosci; 2018; 12(2): 50-105.

5. Vik-Mo AO, Bencze J, Ballard C, Hortobágyi T, Aarsland D. Advanced cerebral amyloid angiopathy and small vessel disease are associated with psychosis in Alzheimer's disease. J Neurol Neurosurg Psychiatry. 2019; 90(6): 728-730.

6. Wallace L, Theou O, Rockwood K, Andrew MK. Relationship between frailty and Alzheimer's disease biomarkers: A scoping review. Alzheimers Dement (Amst). 2018; 10(3): 394-401.

7. Md. Reyad-ul-Ferdous, D. M. Shamim Shahjahan, Sharif Tanvir, Mohsina Mukti; Present Biological Status of Potential Medicinal Plant of Amaranthus viridis: A Comprehensive Review. 2015; 3(5): 12-17.

8. Sowjanya Pulipati, Puttagunta Srinivasa Babu, M Lakshmi Narasu Phytochemical and Pharmacological potential of Amaranthus viridis L. 2014; 6(12): 322-326.

9. Walter E. Thomas, Ian C. Burke, Janet F. Spears, John W. Wilcut. Influence Amaranth (Amaranthus viridis) Germination. Weed Science. 2017; 54(2): 316-320.

10. Ali Haider, Muhammad Ikram, Urooj Fatima, Asma Javed Haider Pharmaceutical Activity of Medicinal Plant Amaranthus viridis Linn. Due to its Chemical Constituents: A Review Bioeduscience. 2023; 7(2): 143-148.

11. Morris RG, Garrud P, Rawlins JN, O'Keefe J. Place navigation impaired in rats with hippocampal lesions. Nature. 1982; 58(8): 681-683.

Received on 13.07.2024 Modified on 27.07.2024

Res. J. Pharmacology and Pharmacodynamics.2024;16(3):161-167.

DOI: 10.52711/2321-5836.2024.00028

Pharmacological Evaluation of Amaranthus viridis Linn leaves Extract for Anti Alzheimer’s Activity in Rat Models