1. INTRODUCTION:

The most prevalent cause of dementia globally, Alzheimer's disease (AD) is a progressive neurological illness that affects millions of people and places a significant strain on families, caregivers, and healthcare systems¹. Clinically, AD is typified by a progressive deterioration in cognitive abilities, memory loss, and behavioural abnormalities that eventually result in total dependence and death². It is characterized pathologically by the buildup of intracellular neurofibrillary tangles made of hyperphosphorylated tau protein, extracellular amyloid-beta (Aβ) plaques, synaptic dysfunction, and extensive neuronal death. Even after decades of study, the exact cause of AD is still unknown and complex, involving age-related biochemical alterations, environmental triggers, and genetic predisposition³. Neuronal degeneration is primarily caused by oxidative stress and mitochondrial dysfunction, two of the many processes linked to AD pathogenesis. Neurons are extremely energy-dependent cells that rely on oxidative phosphorylation in the mitochondria to meet their metabolic needs. The mitochondrial bioenergetics are seriously disrupted in AD, which results in decreased ATP synthesis, decreased electron transport chain (ETC) activity, and elevated reactive oxygen species (ROS) production⁴. These changes start apoptotic pathways, interfere with cellular signalling, and interfere with synaptic transmission. Oxidative damage to lipids, proteins, and nucleic acids occurs when the brain's natural antioxidant defence systems are overloaded. Neurodegeneration and cognitive decline are accelerated by this vicious cycle of oxidative stress and mitochondrial dysfunction. Multi-targeted treatment techniques are gaining popularity due to the complexity of AD and the ineffectiveness of monotherapeutic approaches that focus on individual pathology characteristics. The capacity of natural compounds to simultaneously affect several pathways has drawn attention, especially those with pleiotropic effects⁵. Centella asiatica (CA), also referred to as gotu kola, is a medicinal herb that has been utilized in Southeast Asian, Chinese, and Ayurvedic medicine for a long time⁶. CA has long been known to have anxiolytic, wound-healing, and cognitive-enhancing effects. Its neuroprotective potential has been investigated recently in relation to neurodegenerative illnesses, such as AD⁷. CA rich phytochemical makeup, which mostly consists of triterpenoids such as asiaticoside, madecassoside, asiatic acid, and madecassic acid, is responsible for its pharmacological efficacy. These substances have strong anti-inflammatory, neuroprotective, and antioxidant qualities⁸. Research has demonstrated that CA can alter important physiological processes related to neuroinflammation, oxidative stress response, and mitochondrial function. By maintaining mitochondrial membrane potential, increasing ATP synthesis, and stimulating mitochondrial biogenesis by activating peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), CA notably improves mitochondrial bioenergetics. These processes lessen vulnerability to apoptotic signals and aid in the restoration of neuronal energy metabolism⁹. A master regulator of antioxidant defence, CA also activates the nuclear factor erythroid 2–related factor 2 (Nrf2) pathway in addition to its effects on mitochondrial activity. When Nrf2 is activated, more genes that encode antioxidant enzymes like glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD) are transcriptionally active. In order to neutralize ROS, preserve redox equilibrium, and shield neurons from oxidative injury, these enzymes are essential¹⁰. Additionally, CA promotes the production and recycling of glutathione (GSH), a crucial intracellular antioxidant that strengthens the brain's defences against oxidative stress. In addition to its antioxidant and mitochondrial functions, CA has anti-inflammatory and anti-apoptotic properties. By blocking the activation of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathways, it lowers the expression of pro-inflammatory cytokines such as interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-α)¹¹. CA helps maintain the structure and function of neurons by reducing microglial activation and inhibiting neuroinflammatory pathways. By stabilizing mitochondrial membranes and preventing caspase-3 activation, it also stops neuronal death. Although CA neuroprotective properties are strongly supported by preclinical studies, little is known about how exactly it modulates antioxidant pathways and mitochondrial bioenergetics in the context of AD. The majority of research has been on behavioural enhancements or general cognitive results, offering little mechanistic understanding of mitochondrial dynamics and redox regulation. To further bridge the gap between lab and bedside, thorough translational research is required as clinical validation of CA's effectiveness in AD patients is still in its infancy¹².

This review is to methodically investigate the molecular pathways that CA uses to provide neuroprotection in AD, with an emphasis on antioxidant pathways and mitochondrial bioenergetics. By combining data from limited clinical studies, in vitro, and in vivo research, we aim to present a thorough grasp of CA's therapeutic potential and applicability in the creation of multi-targeted AD therapies. We also draw attention to the necessity of more study to confirm efficacy in human populations, enhance bioavailability, and optimize dosage¹³.

2. Phytochemical constituents of Centella asiatica:

Ayurveda, Traditional Chinese Medicine (TCM), and Indonesian jamu all hold CA, also referred to as gotu kola, in high regard as a therapeutic herb¹⁴. Its broad and varied phytochemical profile is thought to be responsible for its therapeutic promise in neurological illnesses, including AD. CA is a promising option for a multi-targeted intervention in AD because of the synergistic effects of these bioactive substances, which have anti-inflammatory, antioxidant, and neuroprotective properties¹⁵.

Triterpenoids, the most abundant family of chemicals in CA, have been thoroughly investigated for their potential to modulate oxidative stress and mitochondrial function¹⁶. Among these, the glycosides madecassoside and asiaticoside are well-known for their capacity to affect neuronal signalling and penetrate the blood-brain barrier¹⁷. A triterpenic derivative, Asiatic acid promotes the integrity of the mitochondrial membrane and has potent free radical scavenging properties. These substances inhibit apoptosis and mitochondrial fragmentation in addition to increasing ATP synthesis. Another triterpenoid that aids in cellular repair and anti-inflammatory reactions is madecassic acid¹⁸. CA contains strong antioxidant flavonoids like kaempferol and quercetin in addition to triterpenoids. These compounds increase natural antioxidant enzymes, decrease lipid peroxidation, and neutralize reactive oxygen species (ROS). By promoting redox equilibrium and shielding neuronal membranes from oxidative damage, phenolic acids such as caffeic acid and chlorogenic acid further improve CA's antioxidant profile. Additional components like volatile oils and sterols aid in improving membrane stability and bioavailability. The adaptogenic and cognitive-enhancing properties of saponins, such as brahmoside and brahminoside, may enhance the neuroprotective benefits of CA¹⁹. Table 1 below summarizes the key phytochemical classes, their major constituents, and associated pharmacological actions^20-22.

Table 1: Phytochemical Composition of CA.

Compound Class	Key Constituents	Pharmacological Actions
Triterpenoids	Asiaticoside, Madecassoside, Asiatic acid, Madecassic acid	Antioxidant, neuroprotective, anti-inflammatory, mitochondrial support
Flavonoids	Quercetin, Kaempferol	Free radical scavenging, anti-inflammatory and enhances antioxidant enzyme activity
Phenolic acids	Caffeic acid, Chlorogenic acid	ROS neutralization, lipid peroxidation inhibition
Sterols	β-sitosterol	Membrane stabilization, anti-inflammatory effects
Volatile oils	Terpenes, sesquiterpenes	Enhances bioavailability, contributes to overall therapeutic synergy
Saponins	Brahmoside, Brahminoside	Cognitive enhancement, adaptogenic effects

In pharmacological research, standardized extracts like TECA (Titrated Extract of Centella asiatica) are frequently used to guarantee constant concentrations of these bioactive substances. Numerous in vitro and in vivo models of neurodegeneration have shown that these extracts are effective, confirming the phytochemical composition of CA's therapeutic value. Optimizing CA's application in Alzheimer's treatment requires an understanding of its molecular variety. Future investigations ought to concentrate on separating distinct substances, examining their pharmacokinetics, and assessing how well they work together in clinical contexts.

3. Pathophysiology of Alzheimer’s Disease:

AD is a complex neurological disease characterized by behavioural abnormalities, memory loss and progressive cognitive deterioration. The complicated pathophysiology of AD includes a series of cellular and molecular processes that culminate in brain atrophy and neuronal death²³. To understand how therapeutic medicines like CA may intervene in the progression of disease, one must have a thorough understanding of the underlying pathophysiology and pathway related to the consequences of AD, which are illustrated in Table 2. Amyloid-beta (Aβ) peptides build up to create extracellular plaques, one of the most well-studied and early characteristics of AD. β-secretase and γ-secretase sequentially cleave the amyloid precursor protein (APP) to produce these peptides. Because they cause oxidative stress, interfere with synaptic transmission, and induce inflammatory reactions, the oligomeric forms of Aβ are especially hazardous²⁴. Moreover, Aβ buildup disrupts mitochondrial activity, resulting in decreased ATP synthesis and elevated reactive oxygen species (ROS) production. Hyperphosphorylated tau protein forms neurofibrillary tangles (NFTs), another characteristic of AD. In neurons, tau typically stabilizes microtubules. However, aberrant phosphorylation in AD leads tau to collect and detach, impairing axonal transport and causing neuronal dysfunction. Synaptic degeneration and anomalies in the mitochondria are intimately associated with tau disease. The pathophysiology of AD is significantly influenced by mitochondrial dysfunction. Since mitochondrial oxidative phosphorylation is a major source of energy for neurons, any interference with this process can have a significant impact on brain activity²⁵. Reduced membrane potential, aberrant mitochondrial structure, and decreased electron transport chain (ETC) activity are all present in AD. Reduced ATP synthesis, elevated ROS generation, and apoptotic pathway activation result from these alterations. Cellular stress and neurodegeneration are made worse by mitochondrial fragmentation and compromised mitophagy. In AD, oxidative stress both causes and results in mitochondrial dysfunction. Overproduction of ROS impairs cellular function and increases inflammation by damaging proteins, lipids, and DNA. A pro-oxidant environment results from an overabundance of the brain's antioxidant defence system, which includes enzymes such as glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD). Aβ toxicity, tau hyperphosphorylation, and synaptic loss are all influenced by this oxidative imbalance²⁶. Another crucial element of AD pathogenesis is neuroinflammation. Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) are pro-inflammatory cytokines released by activated microglia and astrocytes that increase neuronal injury. Prolonged inflammation speeds up the course of disease, damages neurogenesis, and interferes with the blood-brain barrier²⁷. Oxidative stress, inflammatory signalling, and mitochondrial malfunction all contribute to apoptosis, or programmed cell death. in areas vital to memory and cognition, such as the cortex and hippocampus. Apoptosis, oxidative stress, neuroinflammation, mitochondrial dysfunction, tau and amyloid pathology, and other factors interact intricately in the pathophysiology of AD. A vicious cycle of neuronal injury is produced by these interrelated processes. Treatment approaches that target several facets of this cascade, as those provided by CA, have the potential to reduce or stop the progression of the disease²⁸.

The main cause of AD, a progressive neurodegenerative disease marked by memory loss, cognitive decline, and behavioural abnormalities, is neuronal death in particular brain regions. Amyloid-β (Aβ) plaques outside of neurons and neurofibrillary tangles (NFTs) made of hyperphosphorylated tau protein inside neurons are the disease's primary clinical characteristics. Amyloid precursor protein (APP) processing goes awry at the start of the disease²⁹. The plaques cause oxidative stress, microglial activation, neuroinflammation, and disruption of neuronal transmission. The tau protein, which typically stabilizes microtubules inside neurons, also exhibits aberrant hyperphosphorylation at the same time. Axonal transport is hampered by the ensuing microtubule breakdown, which causes synaptic dysfunction and neuronal death. After aberrant APP cleavage and amyloid-β buildup, tau hyperphosphorylation, neuroinflammation, oxidative stress, and synaptic loss occur leading to eventual neuronal death. Overall, amyloid-β buildup and tau hyperphosphorylation are the first steps in the pathogenic cascade of AD. Hyper phosphorylation of Tau causes synaptic damage and mitochondrial stress leads to loss of function and mitochondrial dysfunction which decreases ATP and increases ROS. Which followed with oxidative stress and neuroinflammation leading to Apoptosis of neurons. Apoptosis leads to cell death cause progressive loss of neurons, particularly in brain regions leads to memory loss, producing, are shown in Figure 1.^30,31

4. Mechanism of Action of CA in Neuroprotection:

The capacity of CA to concurrently control several pathogenic processes is thought to be the reason for its therapeutic success in AD. Apoptosis, oxidative stress, neuroinflammation, mitochondrial malfunction and synaptic failure are some of the hallmarks of AD, a complex neurodegenerative disease³⁴. Through its intervention at multiple crucial molecular checkpoints linked to the course of AD, CA, a medicinal herb rich in triterpenoids such as asiaticoside, madecassoside, asiatic acid, and madecassic acid, has neuroprotective benefits. Enhancement of mitochondrial bioenergetics is one of the main ways that CA provides neuroprotection. In AD, mitochondrial dysfunction results in decreased ATP synthesis, membrane potential loss, and elevated reactive oxygen species (ROS) generation. It has been demonstrated that CA restores oxidative phosphorylation and ATP synthesis by increasing the activity of electron transport chain complexes, especially Complex I and IV. Furthermore, CA maintains mitochondrial membrane potential, avoiding cytochrome c release and depolarisation, two major death triggers³⁵. Crucially, CA stimulates the replication and repair of damaged mitochondria by activating peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), a master regulator of mitochondrial biogenesis. Together, these processes enhance neuronal energy metabolism and lessen susceptibility to apoptotic signals. To combat the oxidative damage that is common in AD, CA activates the body's natural antioxidant defence systems. A key player in this process is the nuclear factor erythroid 2–2-related factor 2 (Nrf2) pathway³⁶. Superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) are among the antioxidant enzymes whose transcription is upregulated as a result of CA-induced nuclear translocation of Nrf2. These enzymes prevent oxidative damage to biological components by neutralizing ROS. Additionally, CA promotes the production and recycling of glutathione (GSH)³⁷, a crucial intracellular antioxidant that improves neuronal resilience and redox homeostasis. The combined antioxidant properties of CA aid in reducing DNA damage, protein oxidation, and lipid peroxidation—all of which are frequently seen in AD brains. CA has strong anti-inflammatory qualities in addition to its impact on oxidative and mitochondrial pathways. A major factor in AD pathogenesis is neuroinflammation, which is fueled by persistent activation of astrocytes and microglia. Pro-inflammatory cytokines including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) are expressed less frequently when CA inhibits the activation of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathways³⁸. Furthermore, CA promotes a change from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype via modifying microglial polarization. This change promotes tissue repair and neurogenesis while also lowering neuroinflammatory cascades. CA helps maintain the integrity of the blood-brain barrier and avoids additional neuronal damage by reducing inflammation. CA is also essential for preventing neuronal apoptosis, which is a result of oxidative stress and mitochondrial malfunction. Caspases, especially caspase-3, are activated in AD, and pro-apoptotic (like Bax) and anti-apoptotic (like Bcl-2) proteins are out of balance, which causes apoptosis³⁹. CA blocks the execution phase of apoptosis and promotes cell survival by upregulating Bcl-2 expression and inhibiting caspase-3 activation. Additionally, CA inhibits the intrinsic apoptotic pathway, maintaining neuronal architecture and function by stabilizing mitochondrial membranes and blocking cytochrome c release. While not the main emphasis of this article, it is important to note that CA also enhances cognition by modulating cholinergic transmission. Acetylcholinesterase (AChE) is inhibited by CA, which raises acetylcholine levels in the synaptic cleft. Cholinergic transmission is improved, which is crucial for learning and memory formation. CA also promotes dendritic development and synaptic plasticity, which strengthens its contribution to cognitive enhancement. By improving mitochondrial bioenergetics, triggering antioxidant defences, reducing neuroinflammation, preventing apoptosis, and promoting synaptic function, CA works in a variety of ways. CA is a viable option for the creation of integrative treatment approaches for AD because of its multi-targeted activities. Through it improves mitochondrial activity, CA, a medicinal herb with neuroprotective qualities, helps treat AD. By entering neural cells and promoting mitochondrial activity, CA bioactive chemical components enhance mitochondrial bioenergetics. The PGC-1α (Peroxisome proliferator-activated receptor gamma coactivator 1-alpha) pathway⁴⁰, a crucial regulator of energy metabolism and mitochondrial biogenesis, is stimulated by this increase. PGC-1α activation improves the mitochondrial respiratory cycle's efficiency, which raises ATP production and supplies the energy required for neuronal survival and function. CA has several positive benefits on the health of neurons due to enhanced mitochondrial function and energy generation. First, by preserving mitochondrial integrity and lowering oxidative stress, it promotes neuronal survival by preventing neuronal death. Second, because it encourages neuroprotection and blocks inflammatory signalling pathways in the brain, improved mitochondrial activity helps to lower neuroinflammation. Furthermore, promoting neurotransmitter release, receptor binding, and postsynaptic response, all of which improve signal transmission and memory formation, leads CA increase’s synaptic function. Overall, the chemical constituent of CA enters the cell and enhances the mitochondria function which improves bioenergetics, leads to PGC-1α activation and enhances the cycles of mitochondria which increases ATP synthesis⁴¹. Enhancement of mitochondrial function leads to activation of neuroprotection which reduces neuroinflammation and also prevents neuronal apoptosis and improves neuronal function. Synaptic functions such as signal initiation, neurotransmitter release, binding to receptors and postsynaptic response get increased, leading to memory enhancement. Improvement in memory leading to treatment of AD is displayed in Figure 2⁴².

6. Research Gaps and Future Directions:

Although Centella asiatica (CA) is becoming more and more popular as a neuroprotective agent, there are still several important gaps in the literature that restrict its therapeutic application in AD. These deficiencies are recognised and filled in this review, which also suggests important avenues for further study⁴⁸.

1. Limited Clinical Validation:

There are very few randomized controlled trials (RCTs) that directly assess CA's effectiveness in AD patients; the majority of research on the topic is limited to in vitro and animal models. The majority of the clinical data now available evaluates cognitive enhancement in healthy older adults or those with mild cognitive impairment (MCI), without evaluating disease-modifying effects. Well-designed RCTs with diagnosed AD populations that include both cognitive and mechanistic goals should be the focus of future studies⁴⁹.

2. Incomplete Pharmacokinetic and Bioavailability Data:

The bioactive components of CA have limited blood-brain barrier (BBB) penetration and poor oral bioavailability, especially triterpenoids such as asiatic acid and asiaticoside. Despite the potential of bioenhancers and nanoparticle-based delivery systems, thorough pharmacokinetic profiling in humans is still absent. Future research should evaluate sophisticated formulations for CNS targeting and concentrate on absorption, distribution, metabolism, and excretion (ADME) characteristics⁵⁰.

3. Variability in Extract Composition:

There are major variations in plant source, extraction technique, and standardisation processes; there is a significant amount of heterogeneity in the composition of CA extracts used across research. Clinical comparability and reproducibility are hampered by this diversity. To guarantee consistency and therapeutic dependability, future studies must prioritise the use of standardised extracts, like TECA, with thorough phytochemical profiling⁵¹.

4. Lack of Mechanistic Biomarker Integration:

There are a few research investigations that link biological processes like antioxidant enzyme activity or mitochondrial enhancement to clinical outcomes like neuroimaging biomarkers or memory function⁵². To prove causation, future studies should combine behavioural and cognitive evaluations with mechanistic biomarkers (such as ATP levels, ROS indicators, and inflammatory cytokines)⁵³.

5. Underexplored Synergistic Potential:

Since AD is complex, monotherapy might not be enough to stop the disease's progression. Little is known about how CA might work in concert with other neuroprotective substances (like curcumin or resveratrol), lifestyle changes (like exercise or diet), or prescription medications (like donepezil). Examining combo treatments may improve effectiveness and increase their clinical usefulness⁵⁴.

6. Absence of Structure–Activity Relationship (SAR) Studies:

It's unknown how each phytoconstituent specifically contributes to CA's medicinal benefits. The best lead compounds with anti-inflammatory, antioxidant, and mitochondrial qualities must be found through structure activity relationship (SAR) research⁵⁵. Cutting-edge technologies like network pharmacology, transcriptomics, and metabolomics can help rational drug design and speed up this process. There is strong evidence that CA is a multi-targeted neuroprotective agent in relation to Alzheimer's dementia AD⁵⁶. CA deals with multiple key pathogenic aspects of AD through a variety of pharmacological activities, including improving mitochondrial bioenergetics, triggering antioxidant defences, reducing neuroinflammation, stopping neuronal death, and promoting synaptic function. Preclinical research continuously shows how effective it is at maintaining neuronal integrity, redox balance, and cognitive function. Despite its limitations, preliminary clinical data point to positive effects on mood and cognition along with a good safety record⁵⁷. The molecular insights, experimental results, and translational issues related to CA have been methodically compiled in this study⁵⁸. While suggesting future options including standardized formulations, biomarker-integrated trials, and synergistic medicines, it also identifies important research gaps, such as low bioavailability, inadequate clinical validation, and variability in extract composition. This study offers a basis for developing CA based therapies in AD by connecting molecular mechanisms with therapeutic potential. It also stimulates additional investigation through thorough clinical and pharmacological research. To sum up, CA has potential as a disease-modifying agent for Alzheimer's treatment in addition to being a cognitive enhancer. Its incorporation into contemporary neuropharmacology could open the door to safer plant-based substitutes for the treatment of neurodegenerative diseases⁵⁹.

CONCLUSION:

Centella asiatica inhibits various types of pathogenic pathways, most notably oxidative stress and mitochondrial dysfunction, and exhibits significant promise as a neuroprotective substance against Alzheimer's disease. Its bioactive components, particularly madecassoside and asiaticoside, preserve membrane integrity, boost mitochondrial bioenergetics, and promote biogenesis by activating PGC-1α. By lowering ROS generation, lipid peroxidation, and neuronal death, concurrent Nrf2 pathway activation enhances endogenous antioxidant defences. In preclinical research, these combined effects result in improved cognitive results and decreased neuroinflammation. Despite the lack of clinical confirmation, the herb's favourable safety profile and multitargeted mechanism of action highlight its potential as a preventative or supplementary therapy approach for Alzheimer's disease. In order to completely prove Centella asiatica's therapeutic effectiveness in neurodegenerative diseases, future research should concentrate on carefully planned clinical trials, extract formulation standardization, and further explanation of particular molecular interactions.

Author Contribution:

The authors confirm their contribution to the paper as follows:

Writing, original drafting manuscript: Renuka Ekka

Study conception: Shashikala Bhagat

Data collection: Shubham Kumar Sahu

Validation and supervision: Bharti Ahirwar

All authors reviewed the results and approved the final version of the manuscript.

ACKNOWLEDGMENTS:

The authors are grateful to the Department of Pharmacy, Guru Ghasidas Vishwavidyalaya University for their cooperation and for providing institutional facilities.

CONFLICT OF INTEREST:

None

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Received on 03.11.2025 Revised on 27.11.2025

Accepted on 13.12.2025 Published on 31.01.2026

Available online from February 07, 2026

Res. J. Pharmacognosy and Phytochem. 2026; 18(1):96-105.

DOI: 10.52711/0975-4385.2026.00014

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Creative Commons License.

Pathological Feature	Key Events	Consequences
Amyloid-beta Accumulation	Aβ aggregation, plaque formation, synaptic disruption	Neurotoxicity, inflammation, mitochondrial damage
Tau Hyperphosphorylation	Detachment from microtubules, NFT formation	Axonal transport failure, synaptic dysfunction
Mitochondrial Dysfunction	Decreased ATP, increased ROS, membrane depolarization, impaired dynamics	Energy deficit, apoptosis, oxidative stress
Oxidative Stress	ROS overproduction, antioxidant depletion	Lipid/protein/DNA damage, mitochondrial injury
Neuroinflammation	Microglial activation, cytokine release	BBB disruption, neurodegeneration, tau exacerbation
Apoptosis	Caspase activation, Bax/Bcl-2 imbalance	Neuronal death, cognitive decline

Study Type	Model/System	Key Findings	Mechanistic Insights
In Vitro	SH-SY5Y, PC12 neuronal cells	Increased Cell viability, decreased ROS, increased caspase-3, and increased mitochondrial potential	Antioxidant activity, mitochondrial stabilization
In Vitro	Aβ-induced toxicity models	Reduced Aβ aggregation, increased neurite outgrowth	Neuroprotection, synaptic regeneration
In Vivo	Scopolamine-induced AD in rats	Enhanced Memory retention, reduced lipid peroxidation, increased SOD, catalase and GSH	Cognitive enhancement, oxidative stress reduction
In Vivo	Aβ-injected mice	Reduced TNF-α, IL-1β, IL-6, high Bcl-2, reduced caspase-3	Anti-inflammatory and anti-apoptotic effects
In Vivo	Transgenic AD mouse models (APP/PS1)	Enhanced ATP levels, improved mitochondrial morphology and reduced microglial activation	Mitochondrial bioenergetics, neuroinflammation modulation