Approaches in treatment of PD:-

Novel drug delivery systems for the treatment of PD¹³

Drug	Dose	Formulation	Trade name (Manufacturer)
LD/carbidopa	100/25 mg 100/10 mg 250/25 mg	Orally disintegrating tablets	Parcopa (Schwarz Pharma)
LD/carbidopa	20 mg/5 mL	Suspension of microionised LD/carbidopa	Duodopa (Solvay, Neopharma AB)
COMT inhibitors:
Tolcapone	100/200 mg	Oral Film-coated tablets	Tasmar (Valeant Pharmaceuticals)
Entacapone	200 mg	Oral Film-coated tablets	Comtan/Comtess (Novartis/Orion)
MAO-B Inhibitors:
Selegiline	5mg	Oral Capsules	Eldepryl (Somerset Pharmaceuticals)
Selegiline	1.25mg	Sublingual disintegrating tablets	Zelapar (Valeant Pharmaceuticals)
Rasagiline	0.5-1mg	Oral Tablet	Azilect (Teva Pharmaceuticals)
Di-hidroergocriptina	5mg	Oral capsules	Daverium (Marvecs Pharma)
Di-hidroergocriptina	10mg	Oral tablets	Daverium (Marvecs Pharma)
Non-ergoline dopamine receptor agonists:
Pramipexole	0.125/0.25/0.5/1 /1.5 mg	Oral tablets	Mirapex (Boehringer Ingelheim Pharmaceuticals)
Ropinirole	0.25/0.5/1/2/3/4/ 5mg	Oral tablets	Requip (GlaxoSmithkline)
Ropinirole	2/4/8 mg	Oral extended-release tablets	Requip XL (GlaxoSmithkline)
Rotigotine	2 mg/24 h 4 mg/24 h 6 mg/24 h 8 mg/24 h	Transdermal patches	Neupro (Schwarz Pharma)
Rotigotine	-	Nasal spray	(Aderis Pharmac. Schwarz Pharma)
Apomorphine	10mg/ml	Subcutaneous injection	Apokyn (Vernalis Pharmaceuticals)
Apomorphine	10mg/ml	Subcutaneous injection	Apo-go PFS (Britannia Pharmaceuticals)
Apomorphine	5mg/ml	Continuous infusion	Apo-go PFS (Britannia Pharmaceuticals)
Apomorphine	10mg/ml	Subcutaneous injection	Apo-go Ampoules (Britannia Pharmaceuticals)
Apomorphine	5mg/ml	Continuous infusion	Apo-go Ampoules (Britannia Pharmaceuticals)
Apomorphine	10mg/ml	Subcutaneous injection	Apo-go Ampoules (Britannia Pharmaceuticals)
Apomorphine	-	Nasal powder	Apomorphine nasal (Britannia Pharmaceuticals)
Apomorphine	-	Sublingual	Apomorphine sublingual (Amarin Corporation)
Apomorphine	-	Pulmonary dry powder	VR040 (Vectura Group plc )
NMDA receptor antagonist:
Amantadine	100mg	Oral tablets	Symmetrel (Endo Pharmac.)
Amantadine	50mg/5ml	Oral syrup	Symmetrel (Endo Pharmac.)
Anticholinergics:
Biperiden	2 mg	Oral tablets	Akineton (Par Pharmaceutical)
Biperiden	4 mg	Oral controlled release tablets	Akineton (Par Pharmaceutical)
Biperiden	2.3 mg/1 mL	Oral solution	Akineton (Par Pharmaceutical)
Biperiden	5 mg/1 mL	Parenteral solution injection	Akineton (Par Pharmaceutical)
Trihexyphenidyl	2 mg	Oral tablets	Artane (Wyethlederle)
Trihexyphenidyl	2 mg/5ml	Oral elixir	Artane (Wyethlederle)
Trihexyphenidyl	5 mg	Oral prolonged release capsules	Artane Retard (Wyethlederle)
Metixene	5mg	Oral tablets	Tremaril (Lpbist.Farmaceutico)
Benztropine	0.5/1/2 mg	Oral tablets	Cogentin (Par Pharmaceutical)
Orphenadrine	50 mg	Oral tablets	Disipal (Yamanouchi Pharma)
Orphenadrine	40 mg/2 mL	Parenteral	Disipal vials (Yamanouchi Pharma)
Bornaprina	4 mg	Oral tablets	Sormodren (Teofarma)
Ergoline DA receptor agonists:
Bromocriptine	2.5mg	Oral Snap tabs	Parlodel (Novartis)
Bromocriptine	5mg	Oral Capsules	Parlodel (Novartis)
Pergolide	0.05/0.25/1mg	Oral Tablets	Permax (Elililly/Amarin)
Cabergoline	1-2mg	Oral Tablets	Cabaser (Pharnacia and Upjohn)
Lisuride	0.2/0.5/1mg	Oral Tablets	Dopergin (Schering)
Lisuride	2.5 μg/h (10 cm2) 5 μg/h (20 cm2)	Transdermal patches	Nenad TDS (Axxonis)

Drug	Formulation	Formulation technique	Reference
Bromocriptine	CS NPs	Ionic gelation	14
Bromocriptine	CS NPs	Ionic gelation	15
Ropinirole HCl	CS NPs	Ionic gelation	16
Levodopa	CS NPs	Ionic gelation	17
Rasagiline	CG NPs	Ionic gelation	18
Urocortin	PEG-PLGA NPs	Double emulsion and solvent evaporation	19
Levodopa	PLGA NPs	Double emulsion	20
bFGF	GNLs	w/w emulsion-Freeze drying	21
Ropinirole HCl	SLN	Emulsification-solvent diffusion	22
Ropinirole HCl	PLN	Solvent emulsion-diffusion	23
Ropinirole	NE and MNE	-	24

Intranasally delivered drugs for PD:

CS NPs: Chitosan nanoparticles; CG NPs: chitosan glutamate nanoparticles; PEG: Poly (ethylene glycol); PLGA: poly (lactic-co-glycolic acid); HCl: hydrochloride; GNLs: gelatin nanostructured lipid carriers; SLN: solid lipid nanoparticles; PLN: polymer–lipid hybrid nanoparticles; NE: nanoemulsion; MNE: mucoadhesive nanoemulsion; bFGF: basic fibroblast growth factor; NS: not specified.

NOSE TO BRAIN DRUG DELIVERY SYSTEM:

Pathways for nasal drug delivery:

Because the olfactory and trigeminal nerve pathways have direct access from the nose to the brain, there is compelling evidence that they play a role in the precise mechanism of drug transport to the brain via the intranasal route^25,26. To transfer the medicine from the nose to the brain, the paths must converge; however, a particular neural pathway may predominate over others, depending on the drug's physicochemical makeup, formulation, and manner of administration through the nose^27,28. Both the olfactory and trigeminal nerves originate in the brain and terminate in the nasal cavity's olfactory neuro-epithelium. Since both nerve paths are most superficially exposed to the area of the central nervous system, they are thought to be the most direct and least intrusive ways to deliver the drug to the brain²⁹

Fig (1). Pathways for nasal drug delivery system

1. Olfactory Pathway:

For the treatment of CNS disorders, drugs can be administered through the olfactory mucosa to reach the brain tissues or CSF²³, which also allows for a quicker beginning of action and the possibility of avoiding the blood-brain barrier³¹. Other parts of the brain, such as the amygdale, cortex, and hypothalamus, are projected onto the olfactory bulb³². Furthermore, these areas allow for precise medication distribution. Because basal cells and neural cells migrate uniformly, medication delivery to the brain is improved. The nasal epithelium prevents toxic chemicals from accessing the brain. Mucus on the nasal epithelium traps toxic or dangerous chemicals, which are then expelled by the movement of cilia. The olfactory epithelium is made up of progenitor cells, supporting cells, and neuronal cells that are joined by stiff junctions²⁵. Drugs are carried throughout the central nervous system by olfactory sensory neurons via axonal transport³³. Transport speed may be significantly impacted by axon diameter, species, transport substance, and other factors³⁴. When a medicine is administered intranasally, it rapidly reaches the central nervous system and olfactory bulb. Drug delivery through the olfactory mucosa is accomplished by both intracellular and extracellular transport pathways. When the mucus gel layer must penetrate, three methods are used: passive diffusion through sustentacular cells, the transcellular route via endocytosis, and the paracellular route²⁹.

2. The Trigeminal Nerve Pathway:

Drugs are transported to the brain via this system, which involves trigeminal nerves. The primary cranial nerve that transmits thermosensory and chemosensory information to the mucosae of the mouth, nose, and eyes is the trigeminal nerve³⁵. The ocular, maxillary, mandibular, and fifth cranial nerves make up the trigeminal nerve³⁶. The olfactory and respiratory mucosae are innervated by these trigeminal nerves, which facilitate the passage of chemicals, especially to the brain stem and the remainder of the brain. There is no connection between the nasal cavity and the trigeminal nerve fiber ends. However, the initial point of entrance is the branches of the trigeminal nerve that feed the dorsal nasal mucosa²⁷. Both the mandibular branch and the brainstem pons receive branches of the trigeminal nerve³¹. Trigeminal pathways are interested in both the rostral and caudal regions of the brain, whereas the olfactory route is exclusively interested in the rostral region³⁷. Intracellular and extracellular transport are components of trigeminal nerve circuits. Numerous investigations have been carried out by many experts to look into the particular data supporting the nasal route of medication administration to the trigeminal nerves³². Fig. (1) illustrates how the many processes involved in drug transport via the nasal route may be realized using a generalized graphical model.

Transport mechanisms for the delivery of drug by nasal route:

The medication must continually strike cilia in order to penetrate the nasal mucosal layer. Cilia movement is regulated by ciliated columnar cells found in nasal epithelium^38,39. In the respiratory region, cilia are motile, while in the olfactory region, they are immotile. Once the medicine has passed past a barrier like cilia, it is transported across the nasal mucosa by a paracellular or transcellular route.

1. Transcellular Transport:

Receptor-mediated endocytosis is one of the main ways that drugs are transported across the blood-brain barrier. The trigeminal ganglions, olfactory bulb, and olfactory epithelium all contain nicotinic acetylcholine receptors. Evidence of receptor-mediated endocytosis has been demonstrated by them. The molecules that cause receptor-mediated endocytosis are between 100 and 200 nm in size. Consequently, it has been demonstrated that particle size plays the most significant role in determining receptor-mediated endocytosis; in addition, the mode of transport is influenced by cell type, surface charge, and particle concentration⁴⁰.

2. Paracellular Transport:

Nasal epithelial cells that are resistant to big molecules and confined by tight connections become permeable due to constant cross-talk between neurons and basal cells⁴¹. To allow paracellular trafficking, stiff connections like this are opened⁴². Few studies provide evidence that most medications are transported through the nasal mucosa to the brain. There are several molecular mechanisms into which endocytosis may be divided, including phagocytosis, micropinocytosis, clathrin-mediated, and clathrin-independent⁴³.

Advantages of nose to brain drug delivery system:^44,45

1. It is a rapid, quick, safe, and non-invasive method to deliver drugs.

2. Prevents breakdown of drugs in the gut, particularly peptide drugs.

3. It improves bioavailability by avoiding gastrointestinal wall metabolism and hepatic first-pass metabolism.

4. Because it circumvents the blood-brain barrier, it delivers drugs specifically to the central nervous system while lowering systemic exposure to the medication and its related systemic adverse effects.

5. A therapeutic agent can be administered by nose-to-brain medication delivery without any modifications.

6. The extremely permeable and vascular nasal mucosa allows for both quick action and sustained medication absorption.

7. Improved compliance of patients since self-administration is also possible with this form of drug administration

8. It offers as a second parenteral route of administration.\

9. Has high bioavailability for low molecular weight drugs.

Limitations of nose to brain drug delivery system:^44,45

1. Quick removal of drug chemicals from nasal cavity through mucociliary clearance.

2. Formulation ingredients used as absorption enhancers can cause mucosal toxicity.

3. Large molecular weight of drugs can lead to reduced permeation across nasal mucosa.

4. Certain medications may cause irritation to the nasal mucosa or may be subject to enzymatic breakdown and metabolism at the mucosal surface of the nasal environment.

5. Nasal congestion secondary to cold or allergic status can impair this route of drug administration.

6. Repeated use of this pathway can cause mucosal infection and damage or anosmia

7. Mechanical loss of the dosage form is caused by inadequate administration technique

8. Mechanisms of drug transport are not known

FORMULATIONS OF ACTIVE COMPONENTS USED VIA NOSE-TO-BRAIN ROUTE:

Antioxidants	Disease	Formulation	Reference
Resveratrol and vitamin E	Parkinson’s disease	Nanoemulsion	46
Naringenin	Parkinson’s disease	CS NPs	47
Naringenin and vitamin E	Parkinson’s disease	Nanoemulsion	48
Genistein	Alzheimer’s / Parkinson’s disease	CS NPs	49
Melatonin	Alzheimer’s / Parkinson’s disease	Gel suspension	50
Catalase	Parkinson’s disease	Exosomes	51

Resveratrol and Vitamin E:

Fig (2). Structure of Resveratrol

Many fruits and vegetables, but especially red grapes, have resveratrol (3,5,40-trihydroxystilbene), a type of the polyphenol chemicals derived from plants. It is characterized by its anti-inflammatory and antioxidant nature.⁵² The antioxidant property of resveratrol, which is due to its free radical scavenging ability, protects cells against oxidative stress.⁵³The nanoemulsions were produced via high-pressure homogenization combined with spontaneous emulsification. The formulations were determined in vitro by globule size, surface morphology, zeta potential, in vitro release, in vitro viscosity release, and ex vivo permeability. Researchers attribute the significant antioxidant activity in the nanoemulsions to the combination of vitamin E and resveratrol's antioxidant properties. Excellent scavenging effectiveness was revealed by the antioxidant activity examined using a DPPH test. Pharmacokinetic analyses revealed a high drug concentration in the brain of Wistar rats when the nanoemulsions were administered nasally. Vitamin E is unquestionably beneficial for creating a formulation with antioxidant action for the brain, according to a number of data points in the literature. For example, some studies have found that people with Parkinson's disease had lower plasma concentrations of vitamin E, while those with Alzheimer's disease have low blood levels of vitamin E.⁴⁶

Naringenin:

Fig (3). Structure of Naringenin

Naringenin (5,7,4-trihydroxyflavanone), the most significant flavonoid, occurs in grapefruits, tomatoes, and a number of other culinary fruits, e.g., citrus plants. Naringenin is endowed with strong anti-inflammatory and antioxidant activity. Low water solubility and gastrointestinal metabolism of naringenin result in negligible bioavailability despite its metal chelating ability and ability to scavenge oxygen-free radicals.⁵⁴

Ionic gelation was employed to prepare naringenin nanoparticles successfully, and the formulation was optimized, characterized, and evaluated. Several process parameters, were considered in an effort to optimize the NAR NPs. The required properties of tiny particle size, low PDI, excellent zeta potential, and high entrapment efficiency for nose-to-brain administration were accomplished when NAR NPs were examined by Zetasizer, TEM, and FESEM. Due to the existence of CS, the positive zeta potential suggested that NAR NPs were stable

The controlled release of NAR from the NPs was proved by the in vitro drug release profile. Compared with NAR solution and NAR NPs, the penetration of NAR and the steady-state flow across the nasal mucosa were both greater. At lower concentration (50 g/mL), NAR NPs were free from any cytotoxicity. In SH-SY5Y cells, NAR NPs exhibited enhanced neuroprotective potential and antioxidant activity against 6-OHDA-induced neurotoxicity. Research using fluorescence microscopy showed that SH-SY5Y cells improved their NP cell uptake. Together, our findings demonstrate that NAR NPs can be administered intravenously as a possible therapy for Parkinson's disease.⁴⁷

Naringenin and vitamin E:-

Naringenin and vitamin E have been used to develop a nanoemulsion that can be delivered from the nose to the brain as a potential therapy for PD. Previous research has demonstrated that co-administration of vitamin E and an extra antioxidant may aid in the treatment of neurodegenerative diseases, such as Alzheimer's disease.⁴⁶ Recently isolated goat nasal mucosa was employed in ex vivo permeation studies using a Franz diffusion, and Wistar rats for animal pharmacokinetic studies. NE medication in combination with levodopa, a standard treatment, was shown to reverse the effects of 6-OHDA on the rats, according to the research.

These impacts encompass enhanced swimming activity, grip strength, and muscle coordination. Thus, by evading first pass metabolism, intranasal delivery of NRG NE shields it from the enzymes metabolizing it in the nose and enhances NRG absorption to the brain. This avoids systemic circulation, enhancing the amount of NRG in the brain and enhancing brain bioavailability⁴⁸.

Genistein:-

Fig(4): Structure of Genistein

The isoflavonoid phytoestrogen genistein is well recognized to have neuroprotective and antioxidant properties⁵⁵. Despite early encouraging results, its limited oral bioavailability and poor water solubility restrict its prospective application in clinical studies. Effective delivery methods that can pass across the blood- brain barrier must be developed and researched for medications of this kind; the intranasal route is especially well-suited for this. Rassu et al. synthesized and described genistein-loaded chitosan nanoparticles for nasal- to-brain administration. To create the nanoparticles, sodium hexametaphosphate was used as a novel cross- linker in the ionic gelation procedure. Pig nasal mucosa was used to investigate ex-vivo permeability in comparison to a drug suspension in a pH 6.5 phosphate buffer solution, and the systems were described in vitro. The PC12 cells were utilized to assess cytotoxicity.

The ionic gelation procedure successfully generated GEN-loaded chitosan nanoparticles by using SHMP as a valid alternative to most traditional cross-linkers. Without substantially changing PC12 cell survival or apoptotic events, the formulation's composition affects the loading efficiency and dimensional properties of the nanoparticles, which can aid GEN's ex vivo transit over the nasal mucosa. These first yet promising results assess the potential utility of these nanocarriers for the nasal delivery of GEN to the brain, notwithstanding the need for more study.⁴⁹

Melatonin:-

Fig(5). Structure of Melatonin

The pineal gland releases the neurohormone melatonin, which is famously used to treat migraine headaches, jet lag, and sleep disorders due to its ability to synchronize the body's rhythms with the day and night cycles⁵⁶. Numerous investigations have revealed that melatonin has neuroprotective and antioxidant qualities against oxidative damage caused by amyloid β-protein in vitro⁵⁷. Numerous studies have revealed that melatonin inhibits the development of beta-sheets and Aβ fibrils⁵⁸ and has neuroprotective effects in vivo in transgenic mice⁵⁹. Enzymes that convert active oxygen species to inactive ones are said to function better when melatonin is present⁶⁰. Melatonin possesses a short half-life and has limited, variable bioavailability, and thus qualifies as a class II drug under the Biopharmaceutics Classification System⁶¹.

To facilitate the delivery of melatonin from the nose to the brain, Babu et al. developed gel suspensions based on Carbopol 934P or carboxymethyl cellulose (medium viscosity grade)⁴⁹. After micro-ionization using the ball-milling process, the medication was added to a gel made from 0.125% carbopol or 1% CMC and 0.1% w/v Tween-80. A Brookfield viscosity meter was used to examine the gels' rheological behavior. Three- dimensional bronchial/tracheal (human-derived) epithelial cell cultures (EpiAirwayTM) were used for permeability tests; these same cell cultures have previously been used in a number of investigations as nasal membrane penetration barriers.^61–63Male Wistar rats were used in the in vivo tests, which compared the intravenous and nasal routes of gel delivery. The Carbopol and CMC gels indicated that melatonin was highly permeable via EpiAirwayTM. Following nasal therapy, melatonin levels in the rats' brain and olfactory bulb were around nine and seven times greater for carbopol and CMC, respectively, than for intravenous melatonin. These investigations, according to the authors, demonstrated that melatonin enters the brain through the olfactory bulb following nasal delivery and suggested that it may have neuroprotective benefits when used to treat Parkinson's and Alzheimer's disorders.

Catalase:-

As a redox enzyme, catalase is one of nature's most potent antioxidants, inactivating millions of liberated radicals per second per catalase molecule throughout a reaction cycle⁶⁵. PD is linked to inflammation in the brain, as was previously mentioned, and brain tissue from PD patients has lower catalase activity⁶⁶. According to recent research, catalase malfunction or deficiency is linked to the pathogenesis of age-related degenerative disorders including Parkinson's and Alzheimer's⁶⁷. However, because the BBB prevents this protein from entering the brain, the development of any therapeutic approach utilizing this enzyme was impeded.

Exosomes with embedded catalase are secreted by nanoformulated catalase-supplied macrophages, as shown by Haney et al.⁶⁸. In view of this discovery, the researchers developed a catalase-containing exosome formulation and proposed its use for PD treatment. When comparing several incorporation techniques, such as sonication, freeze-thaw, exosome extrusion in the presence of catalase, and at room temperature incubation with/without saponin permeabilization, the enzyme was integrated into naïve exosomes ex vivo using bovine liver catalase. Size, antioxidant activity, release, and catalase-loading efficiency were used to describe the formulations. To measure the size of catalase-loaded exosomes, Dynamic Light Scattering (DLS) and Nanoparticle Tracking Analysis (NTA) were used. Based on the enzyme's molecular mass, the naked catalase particles were roughly 9.5 nm in size, which is comparable to the theoretical size of a single protein (10.5 nm). Exosomes loaded with catalase varied from 100 nm to 200 nm in size, while blank exosomes were usually in the range of 100 nm in size. A mouse model of PD was used, where confocal imaging studies were done to explore how exosomes were capable of guiding catalase into inflammatory regions in the brain. Intracranial administration of 6-hydroxydopamine (6-OHDA) into C57BL/6 mice was done in order to induce inflammation within the brain.

1,10-Dioctadecyl-3,3,30,30-tetramethylindo-carbocyanine perchlorate (DIL)-labeled exosomes, a lipophilic fluorescent dye, were administered to the animals intravenously or intranasally 21 days later when inflammation peaked. The mice were euthanized four hours later, and their brain slides were analyzed by confocal microscopy, while the mice were perfused. The results showed that intranasal treatment of exosomes resulted in concentrations greater than those supplied by intravenous injection. The pictures showed how exosomes are distributed throughout the brain, particularly in the frontal lobe and cerebellum. To find out which brain cells exosomes aggregate in, the researchers created brain slides that were co-stained with several cell markers. They discovered that the majority of exosomes are present in endothelial cells, microglia, and surrounding neurons. The authors thus predict that exosome-directed catalase delivery to neurons and microglia inside the inflammatory brain would result in ROS reduction and neuroprotection⁵¹.

FUTURE PROSPECT:-

The creation of neuroprotective preparations including antioxidants as a possible novel therapeutic treatment for neurological illnesses is one of the main objectives of current neuropathological research. It is wished that the solutions of formulations presented here would facilitate the delivery of the antioxidants featured in this review, resulting in clinical studies in the near future. Later preclinical and clinical studies will be able to gain a better understanding of the effect that antioxidants can have within the central nervous system by using the nose-to-brain pathway to bypass pharmacokinetic problems.

Consequently, intranasal delivery of treatment for Parkinson's disease also has numerous challenges ahead and more research is needed to enhance approaches to advancing intranasal therapy for PD from preclinical to widespread clinical applications.

CONCLUSION:

The current study examines the most pertinent research data on bioactive substances that prevent the neuropathological effects of neurotoxic synthetic chemicals (6-OHDA, MPTP, and others) in Parkinson's disease models by actively inhibiting the proinflammatory factor. The BBB, an unavoidable barrier that restricts therapeutic drug transport, restricts the brain availability of available anti-Parkinsonian drugs. In addition, the creation of innovative drugs for PD has been hindered by its complex anatomical organization. Some of the bioavailability problems that still need to be addressed in the case of systemic delivery include the BBB's passage, which is a major barrier to brain targeting; the poor water solubility of the majority of antioxidants; their instability in the gastrointestinal tract; and potential metabolization.

Therefore, formulative and preclinical research in animal models use novel formulations that are delivered through the nose-to-brain route, such as exosomes, polymeric nanoparticles, nanocrystals, and nanoemulsions. Because it enables different medication molecules, nanocarriers, peptides, and stem cells to pass through the blood-brain barrier and reach the central nervous system, intranasal therapy is a noninvasive and successful way to treat PD. It's also convenient and simple, Nose-to-brain delivery of natural bioactive compounds via advanced nanocarrier systems represents a promising therapeutic strategy for PD. Future research should prioritize the translation of these findings into clinical trials, address formulation stability and dosing optimization, and navigate regulatory challenges to establish safety and efficacy in humans

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Received on 01.06.2025 Revised on 11.10.2025

Accepted on 25.12.2025 Published on 22.01.2026

Available online from January 29, 2026

Asian J. Pharm. Res. 2026; 16(1):12-20.

DOI: 10.52711/2231-5691.2026.00002

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

Pathophysiology of PD:-

Diagnosis of PD:-

Approaches in treatment of PD:-

NOSE TO BRAIN DRUG DELIVERY SYSTEM:

Pathways for nasal drug delivery:

1. Olfactory Pathway:

2. The Trigeminal Nerve Pathway:

Transport mechanisms for the delivery of drug by nasal route:

1. Transcellular Transport:

2. Paracellular Transport:

Advantages of nose to brain drug delivery system:^44,45

Limitations of nose to brain drug delivery system:^44,45

FORMULATIONS OF ACTIVE COMPONENTS USED VIA NOSE-TO-BRAIN ROUTE:

Resveratrol and Vitamin E:

Naringenin:

Naringenin and vitamin E:-

Melatonin:-

Catalase:-

FUTURE PROSPECT:-

CONCLUSION:

REFERENCES:

Pathophysiology of PD:-

Diagnosis of PD:-

Approaches in treatment of PD:-

NOSE TO BRAIN DRUG DELIVERY SYSTEM:

Pathways for nasal drug delivery:

1. Olfactory Pathway:

2. The Trigeminal Nerve Pathway:

Transport mechanisms for the delivery of drug by nasal route:

1. Transcellular Transport:

2. Paracellular Transport:

Advantages of nose to brain drug delivery system:44,45

Limitations of nose to brain drug delivery system:44,45

FORMULATIONS OF ACTIVE COMPONENTS USED VIA NOSE-TO-BRAIN ROUTE:

Resveratrol and Vitamin E:

Naringenin:

Naringenin and vitamin E:-

Melatonin:-

Catalase:-

FUTURE PROSPECT:-

CONCLUSION:

REFERENCES:

Advantages of nose to brain drug delivery system:^44,45

Limitations of nose to brain drug delivery system:^44,45