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    Article

    Phytochemical Profiling of Mahapaisachika Ghrita Using GC-MS and Its Potential Neuroprotective Pathways in ADHD

    Brihathi Bala1, Azizahmed Arbar1★, Anantamati Bammagol1, Tejaswini Yarazarvimath1★ Corresponding author

    1. 1Department of Kaumarabhritya, KAHER’S Shri. B.M. Kankanawadi Ayurved Mahavidyalaya, PG Studies and Research Center, Belagavi, Karnataka, INDIA.

    CORRESPONDENCE

    Azizahmed Arbar

    Professor and HOD, Department of Kaumarabhritya, KAHER’S Shri. B.M. Kankanawadi Ayurveda Mahavidyalaya, PG Studies and Research Center, Belagavi-590003, Karnataka, INDIA.

    azizarbar@gmail.com

    ORCID: 0000-0003-4420-1392

    Received: 04-02-2026; Revised: 27-03-2026; Accepted: 15-05-2026.

    Volume 18, Issue 4 · pp. 1547–1553 · PUBLISHED Oct-Dec 2026 · DOI: 10.5530/pres.20260067

    ABSTRACT

    Background Ghrita is one of the most commonly used vehicles of medicine administration in Ayurveda. It owes its widespread usage to its capability to spread and target all organs and tissues within a short duration without altering the primary drug itself. Based on LBDDS (Lipid-Based-Drug-Delivery-Systems), ghrita facilitates enhanced bioavailability and solubilisation for both water and lipid soluble components. Classically in Ayurveda samhitas Mahapaisachika Ghrita is indicated in Unmada, Apasmara, Graha rogas and comprises herbal components such as Jatamansi, Haritaki, shankhapushpi, kapikacchu, vacha among others. Objectives This article aims to explore the biochemical and neuropharmacological effects of Mahapaisachika Ghrita and to highlight its possible key role in Ayurveda by way of management of conditions like ADHD. Materials and Methods Gas Chromatography-Mass Spectrometry of the drug Mahapaisachika Ghrita was conducted to separate, identify and quantify the constituents present in the sample to be used for further interpretation of mode of action of the drug. Results 30 major Phytochemicals along with their Peaks, R. times, area%, CAS and Names were identified through GCMS study of Mahapaisachika Ghrita. Conclusion Chemical constituents found in Mahapaisachika ghrita by GCMS study showed significant effect on reducing neuroinflammation and improved neuroprotection through various neural pathways. If given orally, it may be absorbed and distributed by altering the electrolyte-based transport systems, drug uptake, efflux and disposition and if administered as nasya, could act through lipid-mediated free diffusion directly across the blood brain barrier.

    KEYWORDS

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    FULL TEXT

    INTRODUCTION

    ADHD is a neurobehavioral condition affecting both children and adults characterized by Attention deficit, motor overactivity and motor restlessness and impulsivity. In Ayurveda it is often correlated with Unmada, a condition of the manovaha srotas. Mahapaisachika Ghrita has been mentioned in Caraka Samhita Chikitsasthana Adhyaya 9 Sloka 45-48 (Cakrapanidatta, 2008) with its use in conditions like Unmada, Apasmara and Graha rogas among others. It has also been mentioned in Sahasrayoga Ghrita prakarana 44 (Nishteshwar, 2008).

    It contains a total of 23 drugs processed in Go Ghrita. Those are Jatamansi, Haritaki, Shankhapushpi, Charati, Kapikacchu, Vacha, Trayamana, Agnimantha, Kshriakakoli, Coraka, Katurohini, Vayastha, Varahi, Shatapushpa, Mishreya, Guggulu, Shatavari, Amalaki, Rasna, Gandha Nakuli, Shyonaka, Shalaparni and Vruschikali. It has also been hailed as Buddhi and Smruti Karam as well as Anga Vardhana especially in children (Bala).

    GC-MS is a potent analytical method employed to detect volatile and semi-volatile components in complex herbal formulations. It facilitates possible correlation between chemical compounds and pharmacological effects offering scientific basis for Ayurveda formulations.

    In the present study, The GC-MS analysis of Mahapaisachika Ghrita revealed the presence of various compounds exhibiting neuropharmacological effects by modulating neurotransmitter systems, showing anti-oxidant and anti-inflammatory properties or govern neuronal signalling pathways which are significant in attention and executive function.

    When ghrita is administered orally, gastric lipases start the digestion of the triglycerides into monoglycerides and eventually free fatty acid (Aeri and Tripathi, 2022). The embedded active constituents are dissolved and absorbed better due to ghrita being a lipid-based formulation thereby improving solubility (Jadhav and Tare, 2025). A solubilised solid solution containing microionized particles (Aeri and Tripathi, 2022). The lipid-based drug formulation is thus absorbed and distributed by altering the electrolyte-based transport systems, drug uptake, efflux and disposition (Jadhav and Tare, 2025).

    Ghrita acts like a trojan horse. It transports the active therapeutic constituents beyond the blood brain barrier by one of three mechanisms such as lipid mediated diffusion, rapid carrier-or-receptor mediated transport or crossing the blood brain barrier as a complex to provide restorative and protective effects on the nervous tissue by cleansing the damage through its antioxidant and anti-inflammatory effects and enhancing prime neural signalling molecules (acetylcholine modulation) (Satapathy et al., n.d.).

    Nasya karma facilitates a more targeted absorption of active components when compared with other modes of administration. When ghrita is the solvent administered through the nose, due to its characteristic as a lipophilic compound it is likely absorbed either by the olfactory pathway through the olfactory epithelium at the roof of the nasal cavity (Xinchen et al., 2023). It can then enter the olfactory Sensory neurons or it can diffuse through gaps between cells (Koo et al., 2024). The other pathway involved is the Trigeminal Pathway where the compounds are absorbed along its branches providing a direct path to deeper cerebral regions (Xinchen et al., 2023).

    MATERIALS AND METHODS

    Preparation and Procurement

    The Mahapaisachika Ghrita was prepared and procured from GMP Certified Nagarjuna Pharmacy, Bengaluru.

    Analytical Study

    Mahapaisachika Ghrita was analyzed for its organoleptic parameters such as organoleptic characters and physicochemical standards, preliminary Microbiological testing was carried out in were analysed in AYUSH approved ASU Drug Testing Laboratory of Nagarjuna Pharmacy.

    Gas Chromatography Mass Spectrometry

    Gas Chromatography Mass Spectrometry is a technique used to identify and measure chemicals within a sample. Gas Chromatography separates the different chemicals present in a sample whereas Mass Spectrometry identifies and quantifies chemicals by measuring their weights (mass-to-charge ratios). The entire process includes sample introduction, separation by gas chromatography, detection by Mass Spectrometry and Data Detection.

    Initially the provided sample is introduced by placing it in the instrument. If it is a liquid, it is aptly vaporized. Then the vaporised sample is pushed through a thin tube through which chemicals travel at different speeds based on their specific properties. As each chemical pass through the tube, they all enter the Mass Spectrometer. There they are broken into charged fragments which are then measured. These measurements result in the formation of a pattern which is unique for each chemical. Finally, a graph is produced which shows what chemicals are present and along with each of their quantities.

    The GCMS Study of Mahapaisachika Ghrita was conducted under the following Laboratory Conditions:

    1 g sample was extracted with 10 mL of Acetone and 1 µL extract was injected and the instrument conditions are as follows

    The analysis was done with the instrument Shimadzu, Model-GCMS-QP 2010SE with Helium gas as carrier, capillary column with internal diameter of 0.22 mm and length 40 m.wColumn oven temperature was 80.0ºC and injection temperature was 280.00ºC. Injection mode was Split and flow control mode was linear velocity. Pressure used was 24.2 kPa and total flow 19.5 mL/min with column flow 1.50 mL/min and linear velocity 45.1 cm/sec. Purge flow was 3.0 mL/min and split ratio 10.0. High Pressure Injection, carrier gas saver and splitter hold were off. The column temperature program with an initial temperature of 80.0ºC for 2.00 min the raised to 280.0ºC at 10.00ºC/min and maintained for 10.00 min with a further increase to 330.0ºC at a rate of 5.00ºC/min and held for 3.00 min. The Ion source temperature was 200.0ºC and interface temperature was 300.0ºC. Solvent cut time was 1.40 min. Detector Gain mode was relative to the tuning result. Detector gain was 0.95 kV +0.00 kV and Threshold was 0.

    For Mass Spectrometry, the start time was 2.00 min and end time was 33.00 min. the ACQ mode was on scan with event time of 0.30 sec and scan speed of 1666. Start m/z was 35.00 and End m/z was 500.00. Sample Inlet Unit used was the GC-MS System.

    RESULTS

    Mahapaisachika Ghrita was analysed for its organoleptic parameters such as organoleptic characters, Physicochemical standards, and preliminary Microbiological testing.

    Physicochemical Parameters

    The sample was analysed for organoleptic parameters like Colour, odour and physical parameters like specific gravity and refractive index. It was also tested for its saponification value, Iodine value and Maximum Acid Value.

    Organoleptic Characters and Physicochemical standards are mentioned in Table 1.

    Table 1: Organoleptic Characters and Physicochemical standards.
    TestsResults
    Organoleptic Characters
    FormLiquid
    ColourGreenish in colour
    OdourCharacteristic
    Physicochemical Standards
    Specific Gravity0.917
    Saponification Value232.05
    Acid value (Maximum)1.28
    Loss on Drying0.34%
    Refractive Index1.454

    Preliminary Microbiological Tests are mentioned in Table 2.

    Table 2: Preliminary Microbiological Tests.
    TestsResults
    Aerobic Plate Count<1
    Yeast<1

    The GC-MS analysis of Mahapaisachika Ghrita identified 30 major Phytochemicals along with their Peaks, R. times, area%, CAS and Names. They are listed out in Table 3.

    Table 3: Phytochemicals identified in GC-MS analysis of Mahapaisachika Ghrita.
    Peak#R. TimeAreaArea%HeightCAS#Name
    16.30821409320.32939665556-67-2Cyclotetrasiloxane, octamethyl-
    27.00238830934257.281287032830-0-0Cyclobutane, 1-butyl-2-ethyl-
    38.30626532720.391814816111-11-5Octanoic acid, methyl ester
    415.54930511340.4597988572439-79-33-Ethoxy-1,1,1,7,7,7-hexamethyl-3,5,5-tris(tri
    516.11935096650.521735597111-82-0Dodecanoic acid, methyl ester
    617.53827940330.41142753752957-14-96-Dodecenol
    717.57510754190.1673209340642-43-1cis-7-Tetradecen-1-ol
    817.89215973100.24771320145344-72-52-(2',4',4',6',6',8',8'-Heptamethyltetrasiloxan-2'
    918.59125530380.381507767124-10-7Methyl tetradecanoate
    1020.09862687310.92342479719780-33-72-Ethyl-1-dodecanol
    1120.338394156155.8124692097112-39-0Hexadecanoic acid, methyl ester
    1220.60972324451.0740491850-0-02,6,10-Trimethylundeca-1,3-diene
    1321.0513174040.196842040-0-03,7,11-Trimethyldodec-1-yn-3-yl 2,2,2-trifluor
    1421.5111262800.17543645629-96-91-Eicosanol
    1521.6048142581412.0152164856544-71-8(9E,11E)-Octadecadienoic acid
    1621.6277666383911.3148810079112-62-99-Octadecenoic acid (Z)-, methyl ester
    1721.76960702060.93794157112-61-8Methyl stearate
    1821.91356217180.83289325713038-47-69,11-Octadecadienoic acid, methyl ester, (E,E)
    1921.96149309200.73288345113038-47-69,11-Octadecadienoic acid, methyl ester, (E,E)
    2022.18156283840.83249330313038-47-69,11-Octadecadienoic acid, methyl ester, (E,E)
    2122.541104539441.541603681915-5-9.beta.-Sitosterol acetate
    2222.865718560.083579240-0-0Glutaric acid, di(2-propylpentyl) ester
    2323.0858549250.134761825129-60-2Pentadecanoic acid, 14-methyl-, methyl ester
    2423.16725279760.37108896163321-70-0Octanoic acid, 2-ethylhexyl ester
    2524.488461740.12452785593-45-3Octadecane
    2624.56530316080.4511432371341-38-46-Methylheptyl palmitate
    2725.55915230750.224211780-0-0Oxalic acid, monoamide, N-(4-methoxybenzyl
    2826.11924878750.376995410-0-01,3,5-Cycloheptatriene, 2,4-di-t-butyl-7,7-dim
    2926.6490497931.3422349441560-78-72-Methyltetracosane
    3026.79631264990.46883056646-31-1Tetracosane
    677859226100294406483

    The peak report TIC is shown in Figure 1.

    Figure 1: Peak report TIC.

    The following phytochemicals were identified - Cyclotetrasiloxane, octamethyl-;Cyclobutane, 1-butyl-2-ethyl-; Octanoic acid, methyl ester; 3-Ethoxy-1,1,1,7,7,7-hexamethyl-3,5,5-tris(tri); Dodecanoic acid, methyl ester; 6-Dodecenol; cis-7-Tetradecen-1-ol; 2-(2',4',4',6',6',8',8'-Heptamethyltetrasiloxan-2'; Methyl tetradecanoate; 2-Ethyl-1-dodecanol; Hexadecanoic acid, methyl ester; 2,6,10-Trimethylundeca-1,3-diene; 3,7,11-Trimethyldodec-1-yn-3-yl 2,2,2-trifluor; 1-Eicosanol; (9E,11E)-Octadecadienoic acid; 9-Octadecenoic acid (Z)-, methyl ester; Methyl stearate; 9,11-Octadecadienoic acid, methyl ester, (E,E); 9,11-Octadecadienoic acid, methyl ester, (E,E); 9,11-Octadecadienoic acid, methyl ester, (E,E); beta.-Sitosterol acetate; Glutaric acid, di(2-propylpentyl) ester; Pentadecanoic acid, 14-methyl-, methyl ester; Octanoic acid, 2-ethylhexyl ester; Octadecane; 6-Methylheptyl palmitate; Oxalic acid, monoamide, N-(4-methoxybenzyl); 1,3,5-Cycloheptatriene, 2,4-di-t-butyl-7,7-dim; 2-Methyltetracosane, Tetracosane.

    DISCUSSION

    The blood brain barrier is selectively permeable to lipid soluble substances. Ghrita is a complex fat with herbal constituents which are lipid soluble. Hence, they diffuse directly through the blood brain barrier’s lipid layers and facilitate CNS access. This process is known as Lipid mediated free diffusion

    This study identified the presence of antioxidant, anti-inflammatory and neuroprotective constituents in Mahapaisachika Ghrita which may help in reducing the severity of ADHD symptoms.

    Oleic Acid

    Oleic acid is necessary for the proper development and functioning of the brain. It is used to synthesize myelin phospholipids and acts as a neurotrophic factor by promoting axonal and dendritic growth, enhancing neuronal growth and aggregation alongside the facilitation of synapse formation.

    PET imaging shows evidence of microglial activation in the dorsolateral prefrontal cortex and orbitofrontal cortex in adults with ADHD (Schnorr et al., 2024). Activated microglia release pro-inflammatory cytokines like IL-1β and TNF-α, glutamate and other mediators that can impair neuronal development, myelination and synaptic functioning (Anand et al., 2017). These potentially contribute to ADHD symptoms such as inattention and hyperactivity. Oleic acid is an endogenous agonist of Peroxisome-Activated Receptor Gamma (PPAR-γ) (Honda et al., 2025), a ligand-activated transcription factor belonging to the nuclear receptor superfamily. PPAR-γ agonists are broadly neuroprotective and anti-inflammatory, with the ability to inhibit microglial activation and downregulate pro-inflammatory cytokines such as IL-6 and TNF-α (Priya et al., 2024). Therefore, it addresses the neuroimmune dysregulation in ADHD pathophysiology by limiting neuroinflammation and improving oxidative resilience.

    Docosahexaenoic Acid

    DHA is the main omega-3 fatty acid in the brain and a principal component of neuronal membrane structure required in high concentrations for optimal neuronal functioning (Rodríguez et al., 2019). Supplementation with DHA has been shown to maintain and improve brain functioning by influencing membrane structure, fluidity, signalling pathways, receptor systems, enzyme activities and synaptic plasticity. Several observational studies have suggested that children with ADHD have an abnormal PUFA profile wherein reduced plasma concentrations of DHA and Eicosapentaenoic Acid (EPA) are seen along with lower erythrocyte total n-3 PUFA levels. Greater severity in ADHD symptoms has been linked with low blood levels of DHA and EPA (Chang et al., 2018).

    DHA is the precursor of Docosanoids like Resolvins and Protectins (NPD1). Resolvins help promote the resolution of inflammatory processes by down-regulating NF-κB whereas NPD1 protects neuronal cells from oxidative-stress induced apoptosis (Bradbury, 2011). Reduction of DHA in the brain leads to reduction of both dopaminergic as well as serotonergic transmissions. N-3 PUFAs like DHA modulate neuronal signalling. DHA and its precursor EPA help balance immune functions by reducing membrane arachidonic acid and inhibiting PGE2 synthesis thereby reducing pro-inflammatory signalling. They also act as precursors for anti-inflammatory molecules and inhibit free radical generation and oxidative stress leading to an increase in anti-inflammatory action. DHA also helps in the regulation of several dysregulated biological systems like Hypothalamic-Pituitary-Adrenal Axis (HPA) stress response, Autonomic Nervous System activity and Gut Microbiota Axis (GBA) (Chang, 2021).

    Beta Sitosterol Acetate

    Beta Sitosterol acetate is an esterified derivative of the plant sterol Beta Sitosterol where the hydroxyl group is acetylated increasing the lipophilicity and potentially altering bioavailability. It becomes more fat soluble.

    In ADHD models deficits have been found in visual-spatial working memory tasks as well as memory challenges tied to attentional control failures (Luo et al., 2019). It has also been found that there is reduced mitochondrial respiration, lower ATPase activity, depolarized membrane potential, along with elevated superoxide in frontal cortex-relevant cybrid models playing a part in bio-energetic deficits and impaired pre-frontal dopamine/serotonin signalling. These factors affect symptom severity (Verma et al., 2016).

    Beta Sitosterol improves Spatial Learning and recognition memory by reducing Aβ plaques and BACE1 expression, indirectly addressing shared synaptic dysfunction (Verma et al., 2016). It has the ability to mitigate oxidative/nitrosative stress and enhance mitochondrial function in the Frontal Cortex (Vafaei et al., 2024).

    Lauric Acid, Methyl Ester (Methyl Dodecanoate/Methyl Laurate)

    Methyl Laurate is involved in the inhibition of EGR1 receptor. Early Growth Response 1 is an early gene and transcription factor that plays a key role in synaptic plasticity, neuronal activity, learning, memory, and response to stress and reward. These are the processes often disrupted in ADHD (Duclot and Kabbaj, 2017). EGR1 regulates neuronal plasticity through pathways involving NMDA receptors and Long-Term Potentiation (LTP) in brain regions such as the pre-frontal cortex, hippocampus, striatum, and amygdala, which are implicated in attention, executive function, and dopamine signalling relevant to ADHD (Bristot et al., 2024).

    NF-κB is a transcription factor of prime importance in inflammation, oxidative stress, and immune responses. In ADHD, due to neuronal damage, neuro-inflammation and disrupted signalling in prefrontal and cerebellar cortices, it leads to an overactivation of the NF-κB factor (Zheng et al., 2025). Mast cell activation in ADHD may be a trigger for NF-κB via TLR8, MAPKs, and other mediators, leading to glial interactions, Blood-Brain Barrier breakdown, and HPA axis dysregulation (Song et al., 2020). Trans-fatty acids exacerbate ADHD through microbiota-gut-brain axis disruption which indirectly activates NF-κB-linked immune pathways during critical neurodevelopmental windows (He et al., 2025). An inflammatory ADHD biotype correlates with chronic stress and heightened NF-κB activity, promoting chemokine signalling and IL-17 pathways (Schnorr et al., 2024).

    Methyl Laurate decreases the levels of lipopolysaccharide induced Nuclear Factor κ-B (NF-κB) in murine macrophages found in mice (Sivinski et al., 2020). They have functional similarities with human macrophages in processes like phagocytosis, production of TNF-α and IL-6 as well as the mechanisms of NF-κB pathway activation (Chen et al., 2023).

    Octanoic Acid, Methyl Ester (Methyl Caprylate)

    It is also known as Caprylic acid which is a medium-Chain (C8) Monocarboxylic Saturated Fatty Acid (MCFA) (PubChem, n.d.). It is a straight chain isomer of valproic acid (Altinoz et al., 2020) that provide an alternative energy source (ketone bodies) for neurons (Norgren et al., 2020), supporting mitochondrial function and synaptic activity, which is of particular relevance in conditions with impaired glucose metabolism, as seen in neurodevelopmental disorders like ADHD and Alzheimer’s disease (Chung et al., 2021). Under the conditions of low glucose availability, by the incomplete oxidation of fatty acids ketone bodies are produced which are metabolized by the brain to act as an alternative to glucose (Farah, 2014).

    The small molecular size and high lipophilicity of caprylic acid facilitate its ready penetration across biological membranes, contributing to its high absorption and CNS delivery if administered intranasally as Nasya (Taléns-Visconti et al., 2023). Unlike Long-chain fatty acids, MCFAs can quickly cross the Blood-Brain Barrier, directly penetrate the mitochondrial matrix and have intramitochondrial conversion to Acyl-CoA thioesters and get directly processes by the brain (Fan et al., 2023).

    Linalool and Related Terpenoids

    When ingested linalool is metabolised in the gastro-intestinal system into geraniol, nerol and α-terpineol (Milanos et al., 2017). In rat models, geraniol is found to have sedative and hypnotic activity (A.L et al., 2018). It lowered the protein levels of neuro-inflammatory markers like IL-1β, iNOS, NF-κBp65 and COX-2 as well as down-regulated inflammatory genes like MCP-1, TNF-α, IL-6, IL-1β and IDO-1 (Eman and Abdulmalek, 2022). It was also seen to have reduced the concentration of oxidative damage indicators like malondialdehyde, nitric oxide and xanthine oxidase and boosted the activity of neuronal antioxidant enzymes (Eman and Abdulmalek, 2022). It increased levels of reduced glutathione, catalase, Glutathione-S-Transferase (GST) and Superoxide Dismutase activities (Eman and Abdulmalek, 2022). It also improved learning and memory in the same model (Eman and Abdulmalek, 2022).

    Increased Acetylcholinesterase (AChE) activity leads to hippocampal inflammation ad impaired cholinergic status. Geraniol is found to suppress AChE, thereby improving cognitive abilities (Eman and Abdulmalek, 2022).

    Nerol has been found to have neuroprotective, anti-oxidant, memory enhancing properties, especially in models related to neuro-degeneration (Ghashghaie et al., 2019).

    CONCLUSION

    The identification of compounds such as stearic acid, oleic acid among others through GC-MS analysis emphasizes the therapeutic potential of Mahapaisachika Ghrita in the management of ADHD symptoms through anti-inflammatory and anti-oxidant as well as neuroprotective pathways.

    REFERENCES

    As published

    Showing references and in-text citations exactly as published.

    1. Acharya, V. (2008). Y. T; Cakrapanidatta. Caraka Samhita of Agnivesa Elaborated By Caraka and Drdhabala With the Ayurveda-dipika Commentary. Chaukhamba Surbharati Prakashan.GOOGLE SCHOLAR
    2. Aeri, V, & Tripathi, G. (2022). Science behind ghrita: The lipid-based ayurvedic formulations. Clinical Case Reports International, 6(1375), 1–3.GOOGLE SCHOLAR
    3. A.L, A, Santos, C, Marina, L, de, M, C, & Cintra, R. (2018). R; C, R. F. et Al. Depressant Effect of Geraniol on the Central Nervous System of Rats: Behavior and ECoG Power Spectra. Biomedical Journal, 41(5), 298–305. https://doi.org/10.1016/j.bj.2018.08.008DOIGOOGLE SCHOLAR
    4. Altinoz, M. (2020). A; Ozpinar, A; Seyfried, T. N. Caprylic (octanoic) Acid As a Potential Fatty Acid Chemotherapeutic for Glioblastoma. Prostaglandins, Leukotrienes and Essential Fatty Acids, 159, 102142. https://doi.org/10.1016/j.plefa.2020.102142DOIGOOGLE SCHOLAR
    5. Anand, D, & Colpo, G. (2017). D; Zeni, G; Zeni, C. P; Teixeira, A. L. Attention-deficit/hyperactivity Disorder and Inflammation: What Does Current Knowledge Tell Us? a Systematic Review. Frontiers in Psychiatry, 8. https://doi.org/10.3389/fpsyt.2017.00228DOIGOOGLE SCHOLAR
    6. Bradbury, J. (2011). Docosahexaenoic acid (DHA): An ancient nutrient for the modern human brain. Nutrients, 3(5), 529–554. https://doi.org/10.3390/nu3050529DOIGOOGLE SCHOLAR
    7. Bristot, G, & Feiten, J. (2024). G; Pfaffenseller, B; Hizo, G. H; Valiati, M. F. E; Pinto, J. V. et Al. Early Growth Response 1 (EGR1) Is Downregulated in Peripheral Blood From Patients With Major Psychiatric Disorders. Trends in Psychiatry and Psychotherapy. https://doi.org/10.47626/2237-6089-2023-0749DOIGOOGLE SCHOLAR
    8. Chang, J. (2018). P.-C; Su, K.-P; Mondelli, V; Pariante, C. M. Omega-3 Polyunsaturated Fatty Acids in Youths With Attention Deficit Hyperactivity Disorder: a Systematic Review and Meta-analysis of Clinical Trials and Biological Studies. Neuropsychopharmacology, 43(3), 534–545. https://doi.org/10.1038/npp.2017.160DOIGOOGLE SCHOLAR
    9. Chang, J. (2021). P.-C. Personalised Medicine in Child and Adolescent Psychiatry: Focus on Omega-3 Polyunsaturated Fatty Acids and ADHD. Brain, Behavior, and Immunity - Health, 16, 100310. https://doi.org/10.1016/j.bbih.2021.100310DOIGOOGLE SCHOLAR
    10. Chen, S, & Saeed, A. (2023). F. U. H; Liu, Q; Jiang, Q; Xu, H; Xiao, G. G. et Al. Macrophages in Immunoregulation and Therapeutics. Signal Transduction and Targeted Therapy, 8(1), 1–35. https://doi.org/10.1038/s41392-023-01452-1DOIGOOGLE SCHOLAR
    11. Chung, J. (2021). Y; Kim, O. Y; Song, J. Role of Ketone Bodies in Diabetes-induced Dementia: Sirtuins, Insulin Resistance, Synaptic Plasticity, Mitochondrial Dysfunction, and Neurotransmitter. Nutrition Reviews, 80(4), 774–785. https://doi.org/10.1093/nutrit/nuab118DOIGOOGLE SCHOLAR
    12. Duclot, F, & Kabbaj, M. (2017). The role of early growth response 1 (EGR1) in brain plasticity and neuropsychiatric disorders. Frontiers in Behavioral Neuroscience, 11. https://doi.org/10.3389/fnbeh.2017.00035DOIGOOGLE SCHOLAR
    13. Eman, & Abdulmalek, S. (2022). A. Amelioration of Age-related Multiple Neuronal Impairments and Inflammation in High-fat Diet-fed Rats: the Prospective Multitargets of Geraniol. Oxidative Medicine and Cellular Longevity, 1–, 38. https://doi.org/10.1155/2022/4812993DOIGOOGLE SCHOLAR
    14. Fan, L, Zhu, X, & Borenstein, A. (2023). R; Huang, X; Shrubsole, M. J; Dugan, L. L. et Al. Association of Circulating Caprylic Acid With Risk of Mild Cognitive Impairment and Alzheimer’s Disease in the ADNI Cohort. Journal of Prevention of Alzheimer’s Disease, 10(3), 513–522. https://doi.org/10.14283/jpad.2023.37DOIGOOGLE SCHOLAR
    15. Farah, B. (2014). A. Effects of Caprylic Triglyceride on Cognitive Performance and Cerebral Glucose Metabolism in Mild Alzheimer’s Disease: a Single-case Observation. Frontiers in Aging Neuroscience, 6. https://doi.org/10.3389/fnagi.2014.00133DOIGOOGLE SCHOLAR
    16. Ghashghaie, S, Ghobeh, M, & Yaghmaei, P. (2019). The effect of nerol on behavioral, biochemical and histological parameters in male wistar Alzheimer’s rats. Biomacromolecular Journal, 5(1), 12–22.GOOGLE SCHOLAR
    17. He, N, Zhong, J, Deng, S, Liang, J, Li, Q, & Chen, K. (2025). The impact of trans fatty acids on ADHD in relation to the gut microbiome. Frontiers in Nutrition, 12. https://doi.org/10.3389/fnut.2025.1641574DOIGOOGLE SCHOLAR
    18. Honda, A, Hosoda, A, Kamichatani, W, Ogasawara, M, Miyazaki, S, & Kashiwagi, N. (2025). Et al. Peroxisome Proliferator-activated Receptor Α/δ/γ Activation Profile By Endogenous Long-chain Fatty Acids. International Journal of Molecular Sciences, 26(24), 12020. https://doi.org/10.3390/ijms262412020DOIGOOGLE SCHOLAR
    19. Jadhav, S, & Tare, B. (2025). A review of ghee as bioavailability enhancer and its thermal stabilization by medicinal herbs. International Journal of Pharmaceutical Sciences, 3(10). https://doi.org/10.5281/zenodo.17352108DOIGOOGLE SCHOLAR
    20. Koo, J, Lim, C, & Oh, K. (2024). T. Recent Advances in Intranasal Administration for Brain-targeting Delivery: a Comprehensive Review of Lipid-based Nanoparticles and Stimuli-responsive Gel Formulations. International Journal of Nanomedicine, 19, 1767–1807. https://doi.org/10.2147/IJN.S439181DOIGOOGLE SCHOLAR
    21. Luo, X, Guo, J, Liu, L, Zhao, X, Li, D, & Li, H. (2019). Et al. The Neural Correlations of Spatial Attention and Working Memory Deficits in Adults With ADHD. Neuroimage: Clinical, 22. https://doi.org/10.1016/j.nicl.2019.101728DOIGOOGLE SCHOLAR
    22. Milanos, S, & Elsharif, S. (2017). A; Janzen, D; Buettner, A; Villmann, C. Metabolic Products of Linalool and Modulation of GABA(_A) Receptors. Frontiers in Chemistry, 5. https://doi.org/10.3389/fchem.2017.00046DOIGOOGLE SCHOLAR
    23. Nishteshwar, K, & Vidyanath, R. (2008). Sahasrayogam. (2nd Ed.). Chowkhamba Sanskrit Series Office.GOOGLE SCHOLAR
    24. Norgren, J, Sindi, S, Sandebring-Matton, A, Kåreholt, I, Daniilidou, M, & Akenine, U. (2020). Et al. Ketosis After Intake of Coconut Oil and Caprylic Acid-with and Without Glucose: a Cross-over Study in Healthy Older Adults. Frontiers in Nutrition, 7. https://doi.org/10.3389/fnut.2020.00040DOIGOOGLE SCHOLAR
    25. Priya, D, Hani, U, Haider, N, & Talath, S. (2024). S; Shanmugarajan, D; Prabitha, P. Et Al. Novel PPAR-γ Agonists As Potential Neuroprotective Agents Against Alzheimer’s Disease. RSC Advances, 14(45), 33247–33266. https://doi.org/10.1039/d4ra06330aDOIGOOGLE SCHOLAR
    26. PubChem (n.d.). (N.d.). Octanoic Acid. N.d.GOOGLE SCHOLAR
    27. Rodríguez, C, Garcia, T, Areces, D, Fernández, E, García-Noriega, M, & Domingo, J. (2019). C. Supplementation With High-content Docosahexaenoic Acid Triglyceride in Attention-deficit Hyperactivity Disorder: a Randomized Double-blind Placebo-controlled Trial. Neuropsychiatric Disease and Treatment, 15, 1193–1209. https://doi.org/10.2147/NDT.S206020DOIGOOGLE SCHOLAR
    28. Satapathy, D, Pattnaik, G, & Tripathy, S. (2022). Rational of medicinal ghrita on treatment of CNS disorders. Systematic Reviews in Pharmacy, 13(2). https://doi.org/10.31858/0975-8453.13.2.79-82DOIGOOGLE SCHOLAR
    29. Schnorr, I, Siegl, A, Luckhardt, S, Wenz, S, Friedrichsen, H, Jomaa, E, & H (2024). Et al. Inflammatory Biotype of ADHD Is Linked to Chronic Stress: a Data-driven Analysis of the Inflammatory Proteome. Translational Psychiatry, 14(1). https://doi.org/10.1038/s41398-023-02729-3DOIGOOGLE SCHOLAR
    30. Sivinski, S. (2020). E; Mamedova, L. K; Rusk, R. A; Elrod, C. C; Swartz, T. H; Mcgill, J. M. et Al. Development of an in Vitro Macrophage Screening System on the Immunomodulating Effects of Feed Components. Journal of Animal Science and Biotechnology, 11(1). https://doi.org/10.1186/s40104-020-00497-4DOIGOOGLE SCHOLAR
    31. Song, Y, Lu, M, Yuan, H, Chen, T, & Han, X. (2020). Mast cell mediated neuroinflammation may have a role in attention deficit hyperactivity disorder. Experimental and Therapeutic Medicine, 20(2), 714–726. https://doi.org/10.3892/etm.2020.8789DOIGOOGLE SCHOLAR
    32. Taléns-Visconti, R, Julián-Ortiz, D, & J (2023). V; Vila-Busó, O; Diez-Sales, O; Nácher, A. Intranasal Drug Administration in Alzheimer-type Dementia: Towards Clinical Applications. Pharmaceutics, 15(5), 1399. https://doi.org/10.3390/pharmaceutics15051399DOIGOOGLE SCHOLAR
    33. Vafaei, A, Vafaeian, A, Iranmehr, A, Nassireslami, E, Hasannezhad, Behnam, & Hosseini, Y. (2024). Effects of β‐sitosterol on anxiety in migraine‐induced rats: The role of oxidative/nitrosative stress and mitochondrial function. CNS Neuroscience and Therapeutics, 30(9), e14892. –e14892. https://doi.org/10.1111/cns.14892DOIGOOGLE SCHOLAR
    34. Verma, P, Singh, A, & Nthenge-Ngumbau, D. (2016). N; Rajamma, U; Sinha, S; Mukhopadhyay, K. Et Al. Attention Deficit-hyperactivity Disorder Suffers From Mitochondrial Dysfunction. BBA Clinical, 6, 153–158. https://doi.org/10.1016/j.bbacli.2016.10.003DOIGOOGLE SCHOLAR
    35. Xinchen, Y, Tan, J, & Guan, J. (2023). Lipid-based nanoparticles via nose-to-brain delivery: A mini review. Frontiers in Cell and Developmental Biology, 11. https://doi.org/10.3389/fcell.2023.1214450DOIGOOGLE SCHOLAR
    36. Zheng, M, Yang, Z, He, B, Sun, X, Zhan, Y, & Shao, A. (2025). Et al. GFOD1 Regulates Oxidative Stress-induced Damage in ADHD Via NF-κB Signaling Pathway. Brain Research, 1858, 149605. https://doi.org/10.1016/j.brainres.2025.149605DOIGOOGLE SCHOLAR

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    Bala, B., Arbar, A., Bammagol, A., & Yarazarvimath, T. (2026). Phytochemical Profiling of Mahapaisachika Ghrita Using GC-MS and Its Potential Neuroprotective Pathways in ADHD. Pharmacognosy Research, 18(4), 1547–1553. https://doi.org/10.5530/pres.20260067