Journal of Pharmacology and Clinical Toxicology

A Review on Toxins Mediated Neuro Diseases and Ameliorative Role of Certain Phytochemicals

Review Article | Open Access | Volume 11 | Issue 3

  • 1. Department of Biochemistry, University of Allahabad, India
  • 2. Department of Critical Care and Pulmonary Medicine, KGMU-Lucknow, India
  • 3. Department of Biochemistry, Gyan Vihar University, India.
+ Show More - Show Less
Corresponding Authors
Bechan Sharma, Department of Biochemistry, University of Allahabad, India

According to an estimate, about 6.8 million people die every year as a result of neurological disorders. These disorders arise due to degeneration of nerve cells and disrupt normal brain functions impacting personal and professional behaviour like cognition, retention and neurological functions. Though there are many reasons attributed to the emergence of neurodegenerative diseases like genetic, environmental, age, physiological processes etc. The free radicals are formed in the body as a normal product of aerobic metabolism, but it can also be formed due to increased exposure of environmental toxins like heavy metals (aluminium, arsenic, copper, iron, manganese, zinc, cadmium, lead), pesticides (organochlorines, organophosphates), and chronic inflammations or certain disease conditions. If the turnover of free radicals is not maintained, they ultimately lead to initiation of several diseases such as the hepatic, renal, cardiac, neurodegenerative disorders and many more. Brain cells completely depend on oxygen and glucose for energy requirement the increased free radicals may disrupt this process making the individual susceptible to diseases. In this review we have discussed an update of various aspects of neurodegenerative diseases arising due to environment neurotoxins, intrinsic factors, and their amelioration.


• Neurodegenerative Diseases

• Reactive Oxygen Species

• Blood Brain Barrier

• Bioactive Compounds

• Antioxidants


Gupta A, Pandey R, Singh S, Sharma B (2023) A Review on Toxins Mediated Neuro Diseases and Ameliorative Role of Certain Phytochemicals. J Pharmacol Clin Toxicol 11(3):1179.


According to the World Health Organization (2007), the neurological disorders have affected millions of populations globally. The report says that one billion people suffer all over the world, 50 million suffer from epilepsy and 24 million from Alzheimer, depression, and dementias. This disease affects people in all countries irrespective of age, sex, education, or income. Neurodegenerative diseases arise slowly. In this case, the nerve cells or spinal cord does not respond to the stimulus or takes time for responding due to decrease in signal transduction. Gradually with time, the nerves degenerate and stop functioning (ataxia) or develop sensory dysfunction (dementia). Since these diseases are irreversible, there is no cure. Once the progression starts, it can only be delayed or slowed but cannot be reversed or stopped [1-5]. Alzheimer’s is the most common of all neurodegenerative diseases affecting memory and cognition. In this, the plaques called amyloid plaques, and tau tangles are formed. These amyloid plaques are fragments of a transmembrane protein, ‘amyloid precursor protein’, which helps in neurons growth, survival and repair after injury [6]. Parkinson’s disease arise due to loss of nerve cells of peripheral nervous system involved in coordination and muscle movement. Huntington’s is due to the inheritance of mutated Huntington’s gene (HTT) gene. This HTT gene is characterized by expansion of polyglutamine tract poly Q or CAG nucleotide triplet. These mutated genes form inclusion bodies in neurons damaging molecular motors and axonal transport [7]. Multiple sclerosis is an autoimmune disease resulting in loss of sensation, and mobility. Frontotemporal dementia affects person’s behaviour, and speaking. Progressive supranuclear palsy is due to accumulation of tau proteins affecting movements and balance. Creutzfeldt Jacob is due to prions proteins affecting cognition and neuro behaviour.

It is a well-known fact that free radicals are formed in the body as a normal product of aerobic metabolism, but they can also be formed due to increased exposure of environmental toxins like heavy metals such as lead, arsenic, mercury etc and the xenobiotics such as pesticides. Other factors like lack of physical activity, intake of saturated fatty acids and refined sugars, chronic inflammations, and social factors all contribute to disease initiation causing death of neurons and normal brain functions. Brain cells completely depend on oxygen and glucose for energy. Any deviation from this would cause accumulation of free radicals, which decreases the energy supply to the brain [2]. Hence if the turnover of free radicals is not maintained, it ultimately weakens the immune system leading to initiation of several diseases like hepatic, renal, cardiac, neurodegenerative diseases and many more [8,9]. This review presents an updated account of possible environmental toxins and internal factors responsible for development of neurodiseases. Further, the possible amelioration strategies of neurodiseases have also been discussed.


Poverty in childhood, lack of proper hygiene and education, unresolved health issues / disabilities and sometimes the physical abuses, tortures etc. all make the person to suffer from the neurological diseases [10]. Persons who suffer from non-communicable neurological diseases, need dependency which makes them feel inferior [11]. In a report it is stated that parents of children who have low income and education and low quality of life, all these make their children susceptible for higher incidence of epilepsy [12,13]. According to data of World Health Organization and World Federation of Neurological Disorders, inadequate funding, lack of specialist healthcare professionals and costs of treatments are major barriers to proper care and management of neurological disorders.



The environmental toxins/stress have played major role in emergence of neurodiseases. Chronic exposure of atmospheric pollutants like heavy metals and pesticides, air pollution affects the blood brain barrier, and cognitive functions etc. The severity of disease depends upon dose and duration of exposure. In common heavy metals exposure resulted in increased amyloid plaque deposition in Alzheimer’s and α-synuclein in Parkinsons.

  1. Aluminium (Al): The most common use of Al now days is as food wrappers. Other uses are kitchen utensils, cables, duralamine, an alloy, which has 90% of Al. Its admissible daily intake (ADI) is 1 mg/kg of body weight. It interferes with the metabolism of the neurotransmitteri.e. acetylcholine. It may result into iron deposition on myelin sheaths, increased amyloid plaque proteins, and enhanced oxidative stress [14-16].
  2. Arsenic (As): It is primarily used as an insecticide / herbicide, and hence present in the atmosphere. It dissolves in rain contaminating the ground water. It’s As+3 arsenite form is more toxic than As+5 form [17]. It is very much like phosphate and can replace it in few biological functions [18]. Astrocytic cells are the main brain energy metabolic cells. Arsenic interferes with astrocytic metabolism causing decreased glycolysis and CNS impairments [19-20].
  3. Copper (Cu): It is used in making electrical appliances, wires, copper plating and copper utensils. Increased levels of it causes increased ROS, DNA damage, amyloid plaquesdeposition in Alzheimer. Abnormal prion proteins PrPSc have higher affinity for Cu making it resistant to ubiquinol degradation [21].
  4. Iron (Fe): Excess Fe deposition in a developing brain due to haemolysis may lead to immature blood brain barrier formation and neuron damage or neurodegeneration with brain iron accumulation (NBIA) [22-23].
  5. Manganese (Mn): The main exposure is through food containing Mn. In the environment, it reaches from mining and welding industries. High content of Mn causes the development of Parkinsonism, which is like Parkinsons characterized by lethargies, convulsions, and psychosis [24].
  6. Zinc (Zn): Excess Zn interferes with iron and copper absorption causing apoptosis by unregulated activity of enzymes and antioxidants. Ischemia, retarded mental and physical development all are due to high Zn [25].
  7. Cadmium (Cd): The Cd is a known carcinogen, used in batteries, and alloys. People working in mines or smokers are more often exposed to its adverse effects. It damages the blood brain barrier (BBB) permeability, promotes DNA damage, oxidation and apoptosis [26].
  8. Lead (Pb): The primary source of Pb exposure are batteries and automobile exhaust. It impairs the cognitive functions. According to a study, it stimulates microglia resulting in over production of nitric oxide synthase, interleukin 1 β and tumour necrosis factor causing onset of neurodiseases [27-29].
  9. Pesticides: The chemicals are mainly used as a disinfectant and crop protection from insects. Organochlorines inhibit the γ-amino butyric acid (GABA) by blocking GABA receptors. They alter Na-Ca channel and transporters causing neurotoxicity [30]. Organophosphates inhibit AChE activity irreversibly resulting in convulsions tremors and death [31].

The major risk factors responsible for neurotoxic stimulation are aging, DNA damage, mitochondrial dysfunction, protein misfolding, neuroinflammation, excitotoxicity, extrinsic / intrinsic apoptosis or both and defects in the removal pathways of misfolded proteins via ubiquitin proteosomes [32]. Theses uncontrolled and misfolded proteins in the endoplasmic reticulum and cytosol often work as a precursor for neuro pathologies:

Anatomical differences

It is due to changes in size and shape of neurons, glial cells including astrocytes and microglia. In strokes or formation of amyloid plaques in brain cell, it deforms the structure of the cell. Endothelial cells surrounding glial cells of brain are less permeable to macrophages, hence weak defence system in brain.

Reduction in the level of Dopamine

In Parkinson’s synthesis of catecholamines neurotransmitter, the level of ‘dopamine’ decreases which sends message to the brain for movement, resulting in shaking hands, legs, and which slowly worsens over the period. The precursor amino acid for dopamine is tyrosine and when tyrosine conversion to L-dopa is blocked, dopamine is decreased. The exposure to pesticides such as dieldrin and benomyl has been reported to cause dopamine degeneration and inhibits elimination of dihydroxyphenyl aldehyde a toxic compound of dopamine metabolism [33-35].

Oxidation of myelin sheath by free radical species

The myelin sheath of nerve cells acts as insulator and protects neurons. It is made up of unsaturated fatty acids and protein. Uncontrolled free radicals’ production causes oxidation of lipids, proteins, DNA leading to by-products formations like alcohols, aldehydes, cholesterol oxides, peroxides, ketones which are toxic and weaken our immune system [36]. Deposition of iron on myelin sheaths due to breaking or non-continuity in mitochondrial respiratory chain activates immune system. The activated immune system leads to crossing of blood brain barrier (BBB) by immune cells like T cells, B cells, and macrophages and attacking myelin sheaths. This initiates responses like neuroinflammation, demyelination, loss of grey matter and neuronal cell death [37-39].

Calcium and reactive oxygen species (ROS)

Calcium as an important second messenger interacts with the metalloenzymes leading to ROS production [40, 41]. Both calcium and ROS are interdependent. Though, calcium signalling is regulated by ROS production, calcium signalling is crucial for ROS generation [42]. Thus, increased calcium can cause increased ROS. This crosstalk initiates the pathogenesis of several neurodegenerative diseases and neuronal cells death [43-45].

Excitotoxicity mediated neurodiseases

It is due to over production of glutamate receptors where neurotransmitters show neurotoxic effects. The N-methyl-D aspartate receptors (NMDARs) are a group of three ionotropic glutamate receptors, which may cause increased calcium level, and hence increased ROS resulting into occurrence of the CNS diseases [46]. The glutamate antagonists such as memantine inhibit binding of these receptors with glutamate and hence decrease levels of calcium and ROS [47].


Antioxidants are known to sequester metal ions causing oxidative stress in neurons, thereby halting the disease escalating to neurons. They act as a defence system to neutralize the free radicals mediated acute or chronic adverse effects. The antioxidants (enzymatic and non-enzymatic) work synergistically to combat the effects of the free radical species [48,49].

The role of antioxidants is summarised as following: (i) 17β estradiol, an estrogen, is synthesized in the brain by steroids to protect the neurons; (ii) N acetyl cysteine (NAC) is a glutathione precursor, acts as an antioxidant, and anti-inflammatory agent in neuro-diseases and in mucolytic therapy. NAC increases the levels of cysteine and glutathione working as a scavenger of ROS and free radicals. It also restricts the release of cytokines in immune cell proliferation [50]. NAC may help in glutamatergic neurotransmission controlling neuropsychiatric diseases [51,52]. (iii) The resveratrol is a type of natural phenol produced by plants in response to injury or attack by pathogens. It is present in the skin of grapes, berries and fruits [53]. It decreases oxidative stress, cholinergic neurotransmission, neuronal apoptosis and helps in clearance of amyloid plaque protein [54]. (iv) Carotenoids inhibit apoptosis and ROS mediated mitochondrial dysfunction. They control transcription factors such as Nrf2, and NF-κB regulating apoptosis [55]. (v) Lycopene prevents loss of antiapoptotic proteins i.e. Bcl-2 and Bcl-xL, and inhibits pro-apoptotic proteins like Bax [56]. β-carotene inhibits lipids peroxidation and its lower levels are associated with traumatic brain injury [57]. (vi) Astaxanthin prevents brain oedema, via the NF-κB pathway. It inhibits Na+-K+-2Cl− co-transporter-1 (NKCC1), thus reducing the disruption of BBB and acting as neuroprotector [58].

(vii) Lutein protects neurons from apoptotic death by preventing loss of Bcl-2 and Bcl-xL, and accumulation of Bax. It also prevents ganglionic cells from excess glutamate receptors supressing apoptosis [59]. (viii) Fucoxanthin activates PI3K/ Akt pathway promoting Nrf2 translocation during neurotoxic stimulation [60]. (ix) Omega fatty acids are divided into two categories omega-3 and omega-6 fatty acids. Omega-3 fatty acids comprise α-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Omega-6 consist of linoleic acid (LA) and arachidonic acid (ARA). Among these DHA consisting of 90% of omega 3 fatty acid is responsible for maintaining cellular key processes such as release of neurotransmitters, gene expression, myelination, neuroinflammation and neuronal growth [61,62]. (x) Vitamin E (Tocopherols) plays an important role in central and peripheral nervous system. Its deficiency often leads to ataxia, dysarthria and neuromuscular disorders [63]. It inhibits glutamate induced apoptosis and protects against cerebral ischemia [64,65]. They neutralize unstable lipid peroxyl radicals generated from PUFA. Mutation in the α-Tocopherol transfer protein encoded by gene TPPA develops spinocerebellar ataxia (lack of fine motor control), areflexia, loss of proprioception and finally death [66]. (xi) Melatonin, an amphiphilic substance, secreted by the pineal gland [67] is a known antioxidant, and anti- inflammatory agent inhibiting synthesis of prooxidants while promoting that of antioxidant enzymes. As an anti-inflammatory agent, it inhibits cyclooxygenase-2 and blocks the binding of nuclear factor κB to DNA, thus, reducing the expression of the inducible nitric oxide synthase resulting in decreased synthesis of proinflammatory signals [68].


The Ayurvedic treatments are safe with no side effects. The plant based bioactive molecules help maintain balance among vata, pitta and kapha doshas. In ayurveda, treatment of neuro- logical disorders is called vata vyadhi in which brain tissues dries due to lack of nourishment. Vata vyadhi further has 4 catego- ries (i) Kevala vata (Vata alone), (ii) Samsarga (Vata with Pitta and Kapha), (iii) Avarana (entrapment by other Dosha / Dhatu/ Mala), and (iv) Dhatu Kshaya Janya (neurodegenerative). Me- dicinal plants like Withania somnifera, Bacopa monnieri, Centella asiatica, Mucuna pruriens, Papaver somniferum, Loranthus longi- folia, Aconitum, Cassia occidentalis, Panax ginseng, Hyoscyamus niger, Valeriana, Embilica officinalis, Ferula asafoetida, Datura metel, Avena sativa, Annona squamosa, Acoros calamus, Evolvulus alsinoides, Rosmarinus officinalis, Aegle marmelos, and Rauwolfia serpentine are in use since ancient times for neurological treat- ment [69-101]. In addition to these, ginger, turmeric, black pep- per in diets can also help to reduces the imbalances in vatta, pitta and kapha doshas. The panch karma massage, yoga helps to im- proves circulation, flexibility, and relieving stress. In the Table 1,

Table 1: Plants, their phytochemicals and effects on neurodiseases

S. No.




Part used

Common name

Active compound





Withania somnifera








Withanolide A, withanoside lV, Vl

Regeneration of neuronal axons and sendrites, reconstruction of post/ pre neuronal axons, anti- stress



Bacopa mon- nieri







brahmine, herpestine, saponins (bacosides A, A3, and B and bacopasaponin A to F), D -mannitol, betulinic acid, β-sitosterol, and stigmasterols

Neuroprotective, restores activities of cholinergic enzymes, improved cognitive functions



Centella asi- atica

Umbelliferae (Apiceae)


Whole part


Indian pennywort

Triterpenoids, volatile fatty acids, glycosides, flavo- noids, alkaloids, and tannins, asiaticoside

Inhibiting overactivation of p38 MAPK pathway acting as anti- inflammatory,



Mucuna pru- riens




Whole plant


velvet bean

L-dopa and hallucinogenic tryptamines, and anti-nutri- tional factors (phenols and tannins)

L-dopa act as dopamine precursor, can cross blood brain barrier re- storing neurotransmission



Papaver somniferum



Latex capsule seeds


Oppium poppy

Phenanthrenes (thebaine morphine, codeine, and sanguinarine)

Supress the brain (pain killers), enhance mood acting on special neurons




Loranthus longifolia






alkaloids, flavonoids, tannins, terpenoids, reducing


carbohydrates and cardiac glycosides in aqueous ex- tract


Neuroprotection, anxiety, depres- sion









aconite, monkshood, wolfsbane, leopard's bane, devil's helmet or blue rocket


Aconitine, mesaconitine


Neuronal disorders, pain, inflam- mation






Panax gin- seng






roots and rhi- zomes


Asian ginseng, Chinese ginseng, Japanese gingseng or Korean ginseng



Ginsenosides (Rg1), ginseng polysaccharides, ginseng polypeptides, panaxosides

Antidepressant by enhancement of the BDNF-TrkB signalling path- way, increase acetylcholine levels, anti-depression, anti-Alzheimer's disease, anti-Parkinson's disease and protect neurons




Hyoscyamus niger





henbane, black hen- bane, or stinking night- shade


Hyoscyamine, scopolamine, and tropane alkaloids

blocks the function

of acetylcholine in the brain and antagonizes the muscarinic receptors



Embilica of-








Gallic acid, ascorbic acid, ellagic acid, rutin, quercetin, and catechol,

tannins, epigallocatechin-3-gallat and polyphenols

Neuroprotection, Sleep disorders, sedatives, Anxiety, epilepsy,










Garden heliotrope

actinidine, chatinine, shyanthine, valerianine, and valerine

increased GABA receptors, prevents excitotoxicity, neuronal death








Ferula asa- foetida








Rhizome, tap root




Stinking gum

ferulic acid, umbel-liferone, asaresinotannols, farnesiferols A, B, and C, glucose, galactose, l-arabinose, rhamnose,

and glucuronic acid and volatile oil (3-17%) consisting

of disulfides

(2-butyl propenyl disulfide) with monoterpenes (α- and β-pinene, etc.),

free ferulic acid, valeric acid, and traces of vanillin




Sedative, anti-oxidant


Datura metel


Seeds, leafs


tropane alkaloids, tannins, flavonoids, saponins and


Neuro protection, convulsions










Avena sa- tiva




















β-glucans β-glucan, avenanthramides, tocols, sterols, and avenacosides

increased synthesis of brain growth factors (neurotrophins and the vasodilatory molecule nitric oxide, which play a pivotal role in cerebral blood flow regulation) modulation of neurotransmission and inhibi- tion of the enzymes such as MAO-B and AChE, which catalyse the oxi- dation or hydrolysis of numerous neurotransmitters




Annona squamosa




Seeds,bark, leaves


Sugar apple

diterpenoid alkaloid atisine, oxophoebine, reticuline, isocorydine, methylcorydaldine and, flavonoid quercetin-3-O-glucoside

anti-inflammatory effect through reduction NF-?β and attenuated apoptotic on neural cells through reduction of caspase 3







Acoros cala- mus







Leaves, rhi- zome



sweet flag, sway or

muskrat root



Phenylpropanoids (asarone and eugenol), sterols, triterpene glycosides, triterpenoid saponins, sesquiterpenoids, monoterpenes, and alkaloids



Neuroprotection, enhanced mem- ory power





Evolvulus alsinoides




dwarf morning-glo- ry and slender dwarf morn- ing-glory



Whole plant


Scopoletin, umbelliferone, scopolin and 2-methyl-1,2,3,4-butanetetrol


Improves spatial memory forma- tion, inhibit AChE











Rosmarinic acid, camphor, caffeic acid, ursolic acid, betulinic acid, carnosic acid, and carnosol

Decreased lipid peroxidation in ce- rebral tissues in ischemic patients





Aegle marmelos






Bael fruit


Leaves, bark, roots, fruit, seedss

marmenol, marmin, marmelosin, marmelide, psoralen, alloimperatorin, rutaretin, scopoletin, aegelin, marmelin, fagarine, anhydromarmelin, limonene,

â-phellandrene, betulinic acid, marmesin, imperatorin,

marmelosin, luvangentin and auroptene


Decreased oxidation, neuroprotec- tion










Indian snake- root, devil pepper,

or serpentine




alkaloids of the indole

alkaloid (ajmaline, ajmalicine, reserpine, serpentine), and others


mental diseases, schizophrenia bipolar disorder, epilepsy seizures, insomnia, sleep problems

a brief description of plants, their phytochemicals and effects on neuro diseases is given.


The neurological diseases are like a stigma for a person suffer- ing from it and to the family as well. The society needs to be made aware for no any behavioural discrimination with them. There are many reasons for neuro related problems, but the impact of the disease gets increased by several folds when he or she starts feeling alienated in the society. In order to overcome stigma and discrimination, the awareness among the people about various aspects of such diseases is required. There is an urgent need of carrying out extensive research in this direction, especially about early diagnosis, and effective treatment involving plant based bioactive compounds in addition to the regular therapeutics for the neurological disorders.


The authors are grateful to University of Allahabad for providing facilities for carrying out the present work.

  1. Demopoulos HB, Flamm ES, Pietronegro DD, Seligman ML. The free radical pathology and the microcirculation in the major central nervous system disorders. Acta Physiol Stand Suppl. 1980; 492: 91- 119
  2. Pryor WA. The free-radical theory of aging revisited: A critique and a suggested disease-specific theory. In: H. R. Warner R. N. Butler R. L. Sprott and E. L. Schneider Eds. Modern Biological Theories of Aging. Raven Press: New York. 1987; 89-112.
  3. Richardson JS, Subbarao KV, Ang LC. Biochemical indices of peroxidation in Alzheimer’s and control brains. Trans. Am. Soc. Neurochem. 1990; 21113.
  4. Torbati D, Church DF, Keller JM, Pryor WA. Free radical generation in the brain precedes hyperbaric oxygen-induced convulsions. Free Rad Biol Med. 1992; 13: 101-106.
  5. Youdim MBH, l.avie L. Selective MAO-A and B inhibitors radical scavengers and nitric oxide synthase inhibitors in Parkinson’s disease. Life Sci. 1994; 55: 2077-2082.
  6. Angelo D, Erene M, Rakez K, Saskia C, Milton I, Charles P, Glabe G. Calcium dysregulation and membrane disruption as a ubiquitous neurotoxic mechanism of soluble amyloid Oligomers. J Biol Chem. 2005; 280: 172-194.
  7. De Vos KJ, Grierson AJ, Ackerley S, Miller CC. Role of axonal transport in neurodegenerative diseases. Ann Rev Neurosci. 2008; 31: 151- 173.
  8. Fremont Lucie. Biological Effects of Resveratrol. Life Sciences. 2000; 66: 663-673.
  9. Lepoivre M. Flaman JM. Bobé P, Lemaire G, Henry Y. Quenching of the tyrosyl free radical of ribonucleotide reductase by nitric oxide. J Bio Chem. 1994; 269: 21891-21897
  10. Nabi M, Tabassum N. Role of Environmental Toxicants on Neurodegenerative Disorders. Front Toxicol. 2022; 4: 837579.
  11. Hrastelj J, Robertson NP. Socioeconomic status in neurological disorders: a modifiable risk factor? J Neurol. 2022; 269: 3385-3386.
  12. GBD 2016. Neurology Collaborators. Global regional and national burden of neurological disorders 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2019; 18: 459-480.
  13. Aaberg KM, Gunnes N, Bakken IJ, Sorass CL, Bernsten A, Magnus P, et al. Incidence and prevalence of childhood epilepsy: A nationwide cohort study. Pediatrics. 2017; 139: e201639082017
  14. Durkin MS Yeargin-Allsopp M. Socioeconomic Status and Pediatric Neurologic Disorders: Current Evidence. Semin Pediatr Neurol. 2018; 27: 16-25.
  15. Alasfar RH Isaifan RJ. Aluminum environmental pollution: the silent killer. Environ Sci Pollut Res Int. 2021; 28: 44587-44597.
  16. Klotz K, Weistenhöfer W, Neff F, Hartwig A, van Thriel C, Drexler H. The Health Effects of Aluminum Exposure. Dtsch. Arzteblatt Int. 2017; 114: 653-659.
  17. Verstraeten SV, Aimo L, Oteiza PI. Aluminium and Lead: Molecular Mechanisms of Brain Toxicity. Arch Toxicol. 2008; 82: 789-802.
  18. Chung JY, Yu SD, Hong YS. Environmental source of arsenic exposure. J Prev Med Public Health. 2014; 47: 253-257.
  19. Finnegan PM, Chen W. Arsenic Toxicity: the Effects on Plant Metabolism. Front Physio. 2012; 3: 182.
  20. Beard E, Lengacher S, Dias S, Magistretti PJ, Finsterwald C. Astrocytes as Key Regulators of Brain Energy Metabolism: New Therapeutic Perspectives. Front Physiol. 2022; 12: 825816.
  21. De Keyser J, Mostert JP, Koch MW. Dysfunctional Astrocytes as Key Players in the Pathogenesis of Central Nervous System Disorders. J Neurol Sci. 2008; 267: 3-16.
  22. Desai V, Kaler SG. Role of copper in human neurological disorders. Am J Clin Nutr. 2008; 88: 855S-858S.
  23. Akar E, Ünalp A, Diniz G, Ortac R, Senturk B, Yilmaz O, et al. Investigation of iron’s neurotoxicity during cerebral maturation in the neonatal rat model of haemolysis. Folia Neuropathol. 2015; 53: 262-269.
  24. Pyatigorskaya N, Sharman M, Corvol JC, Valabregue R, Yaha-Cherif L, Poupon F, et al. High nigral iron deposition in LRRK2 and Parkin mutation carriers using R2* relaxometry. Mov Disord. 2015; 30: 1077-1084.
  25. Racette BA. Manganism in the 21st century: the Hanninen lecture. Neurotoxicology. 2014; 45: 201-207.
  26. Mizuno D, Kawahara M. The molecular mechanisms of zinc neurotoxicity and the pathogenesis of vascular type senile dementia. Int J Mol Sci. 2013; 14: 22067-22081.
  27. Wang B, Du Y. Cadmium and its neurotoxic effects. Oxid Med Cell Longev. 2013; 2013: 898034.
  28. Chen P, Miah MR, Aschner M. Metals and Neurodegeneration. F1000Res. 2016; 5: F1000
  29. Zhang M, Liu W, Zhou Y, Li Y, Qin Y, Xu Y. Neurodevelopmental Toxicity Induced by Maternal PM2.5 Exposure and Protective Effects of Quercetin and Vitamin C. Chemosphere. 2018; 213: 182-196.
  30. Kumawat KL, Kaushik DK, Goswami P, Basu A. Acute Exposure to Lead Acetate Activates Microglia and Induces Subsequent by Stander Neuronal Death via Caspase-3 Activation. Neurotoxicology. 2014; 41: 143-156.
  31. Caudle WM. Occupational Exposures and Parkinsonism. Handb Clin Neurology. 2015; 131: 225-239.
  32. Sánchez-Santed F, Colomina MT, Herrero Hernández E. Organophosphate Pesticide Exposure and Neurodegeneration. Cortex. 2016; 74: 417-426.
  33. Zádori D, Klivényi P, Szalárdy L, Fülöp F, Toldi J, Vécsei L. “Mitochondrial disturbances excitotoxicity neuroinflammation and kynurenines: novel therapeutic strategies for neurodegenerative disorders”. J  Neurological Sci. 2012; 322: 187-191.
  34. Goldstein DS, Sullivan P, Holmes C, Miller GW, Alter S, Strong R, et al. Determinants of buildup of the toxic dopamine metabolite DOPAL in Parkinson’s disease. J Neurochem. 2013; 126: 591-603.
  35. Masato A, Plotegher N, Terrin F, Sandre M, Faustini G, Thor DOPAL initiates α Synuclein-dependent impaired proteostasis and degeneration of neuronal projections in Parkinson’s disease. npj Parkinsons Dis. 2023; 9: 42
  36. Zhang J, Pu H, Zhang H, Wei Z, Jiang X, Xu M, et al. Inhibition of Na(+)- K(+)-2Cl(-) cotransporter attenuates blood-brain-barrier disruption in a mouse model of traumatic brain injury. Neurochem Int. 2017; 111: 23-31.
  37. Ermak G, Davies KJ. Calcium and oxidative stress: from cell signaling to cell death. Mol Immunol. 2002; 38: 713-721.
  38. Bradley JL, Blake JC. Chamberlain S, Thomas PK, Cooper JM, Schapira AHV. Clinical biochemical and molecular molecular genetic correlations in Friedreich’s ataxia. Hum Mol Genet. 2000; 9275-9282.
  39. Moosmann B Behl C. Antioxidants as treatment for neurodegenerative disorders. Expert Opin Investig Drugs. 2002; 11: 1407-1435.
  40. Velasco M, Rojas-Quintero J, Chávez-Castillo M, Rojas M, Bautista J, et al. Excitotoxicity: An Organized Crime at The Cellular Level. J Neurol Neurosci. 2017; 3: 193.
  41. Görlach A, Bertram K, Hudecova S, Krizanova O. Calcium and ROS: A mutual interplay. Redox Biol. 2015; 6: 260-271.
  42. Gordeeva AV, Zvyagilskaya RA, Labas YA. Cross-talk between reactive oxygen species and calcium in living cells. Biochemistry (Mosc) 2003; 68: 1077-1080.
  43. Chinopoulos C, Adam-Vizi V. Calcium mitochondria and oxidative stress in neuronal pathology. Novel aspects of an enduring theme. FEBS J. 2006; 273: 433-450.
  44. Sharma N, Nehru B. Characterization of the lipopolysaccharide induced model of Parkinson’s disease: Role of oxidative stress and neuroinflammation. Neurochem Int. 2015; 87: 92-105.
  45. Ferrari CKB. Free radicals lipid peroxidation and antioxidants in apoptosis: implications in cancer cardiovascular and neurological diseases. Biologia. 2000; 55: 581-590.
  46. Torben M, Evan HM. The metabolism of neuronal iron and its pathogenic role in neurological disease: Review. Ann. NY Acad Sci. 2012; 1012: 14-26.
  47. Behl C, Widmann M, Trapp T, Holsboer F. “17-beta estradiol protects neurons from oxidative stress-induced cell death in vitro”. Biochem Biophys Res Commun. 1995; 216: 473-482.
  48. Olney JW. Brain lesions obesity and other disturbances in mice treated with monosodium glutamate. Science. 1969; 164: 719-721.
  49. Yun-Zhong F, Sheng Y, Guoyao Wu. Free radicals antioxidants and nutrition. Nutrition. 2002; 18: 872- 879.
  50. Cadet JL. Free radical mechanisms in the central nervous system: An overview. Int J Neurosci. 1998; 4013-4018.
  51. Omara FO, Blakley BR, Bernier J, Fournier M. Immunomodulatory and protective effects of N-acetylcysteine in mitogen-activated murine splenocytes in vitro. Toxicology. 1997; 116: 219-226.
  52. Deepmala Slattery J, Kumar N, Delhey L, Berk M, Dean O, Spielholz C, et al. Clinical trials of N-acetylcysteine in psychiatry and neurology: A systematic review. Neurosci. Biobehav. Rew. 2015; 55: 294-321.
  53. Tardiolo G Bramanti   P   Mazzon   E.   Overview   on   the   Effects of N-Acetylcysteine in Neurodegenerative Diseases. Molecules. 2018; 23: 3305.
  54. Rege SD, Geetha T, Griffin GD, Broderick TL, Babu JR. Neuroprotectiveeffects of resveratrol in alzheimer disease pathology. Front. Aging Neurosci. 2014; 6: 218.
  55. Salehi B, Mishra AP, Nigam M, Sener B, Kilic M, Sharifi-Rad M, et al. Resveratrol: A Double-Edged Sword in Health Benefits. Biomedicines. 2018; 6: 91.
  56. Park HA, Hayden MM, Bannerman S, Jansen J, Crowe-White KM. Anti- Apoptotic Effects of Carotenoids in Neurodegeneration. Molecules. 2020; 25: 3453.
  57. Hira S, Saleem U, Anwar F, Sohail MF, Raza Z, Ahmad B. beta-Carotene: A Natural Compound Improves Cognitive Impairment and Oxidative Stress in a Mouse Model of Streptozotocin-Induced Alzheimer’s Disease. Biomolecules. 2019; 9: 441.
  58. Werner-Allen JW, DuMond JF, Levine RL, Bax A. Toxic Dopamine Metabolite DOPAL Forms an Unexpected Dicatechol Pyrrole Adduct with Lysines of α-Synuclein. Angew Chem Int Ed Engl. 2016; 55: 7374-7378.
  59. Zhang J, Pu H, Zhang H, Wei Z, Jiang X, Xu M, et al. Inhibition of Na(+)- K(+)-2Cl(-) cotransporter attenuates blood-brain-barrier disruption in a mouse model of traumatic brain injury. Neurochem. Int. 2017; 111: 23-31.
  60. Zhang C, Wang Z, Zhao J, Li Q, Huang C, Zhu L, et al. Neuroprotective Effect of Lutein on NMDA-Induced Retinal Ganglion Cell Injury in Rat Retina. Cell. Mol. Neurobiol. 2016; 36: 531-540.
  61. Lin J, Yu J, Zhao J, Zhang K, Zheng J, Wang J, et al. Fucoxanthin a Marine Carotenoid Attenuates beta-Amyloid Oligomer-Induced Neurotoxicity Possibly via Regulating the PI3K/Akt and the ERK Pathways in SH- SY5Y Cells. Oxid Med Cell Longev. 2017; 2017: 6792543.
  62. ?Park HA, Hayden MM, Bannerman S, Jansen J, Crowe-White KM. Anti-Apoptotic Effects of Carotenoids in Neurodegeneration. Molecules. 2020; 25: 3453.
  63. Avallone R, Vitale G, Bertolotti M. Omega-3 Fatty Acids and Neurodegenerative Diseases: New Evidence in Clinical Trials. Int J Mol Sci. 2019; 20: 4256.
  64. Kemnic TR, Coleman M. Vitamin E Deficiency. StatPearls. StatPearls Publishing; Treasure Island FL USA: 2021.
  65. Icer MA, Arslan N, Gezmen-Karadag M. Effects of vitamin E on neurodegenerative diseases: an update. Acta Neurobiol Exp (Wars). 2021; 81: 21-33.
  66. Regner-Nelke L, Nelke C, Schroeter CB, Dziewas R, Warnecke T, Ruck T, et al. Enjoy Carefully: The Multifaceted Role of Vitamin E in Neuro- Nutrition. Int J Mol Sci. 2021; 22: 10087.
  67. Ulatowski LM, Manor D. Vitamin E and neurodegeneration. Neurobiol Dis. 2016; 84: 78-83.
  68. Claustrat B, Leston J. Melatonin:   physiological   effects   in humans. Neurochirurgie. 2015; 61: 77-84.
  69. Cardinali DP. Melatonin: Clinical Perspectives in Neurodegeneration. Front Endocrinol (Lausanne). 2019; 10: 480.
  70. Mannangatti P, Naidu KN. Indian Herbs for the Treatment of Neurodegenerative Disease. The Benefits of Natural Products for Neurodegenerative Diseases. 2016; 12: 323-336.
  71. Nabi M, Tabassum N. Role of Environmental Toxicants on Neurodegenerative Disorders. Front Toxicol. 2022; 4: 837579.
  72. ?Alasfar RH, Isaifan RJ. Aluminum environmental pollution: the silent killer. Environ Sci Pollut Res Int. 2021; 28: 44587-44597.
  73. Klotz K, Weistenhöfer W, Neff F, Hartwig A, van Thriel C, Drexler H. The Health Effects of Aluminum Exposure. Dtsch. Arzteblatt Int. 2017; 114: 653-659.
  74. Verstraeten SV, Aimo L, Oteiza PI. Aluminium and Lead:Molecular Mechanisms of Brain Toxicity. Arch. Toxicol. 2008; 82: 789-802.
  75. Chung JY, Yu SD Hong YS. Environmental source of arsenic exposure. J Prev Med Public Health. 2014; 47: 253-257.
  76. Finnegan PM, Chen W. Arsenic Toxicity: the Effects on Plant Metabolism. Front. Physio. 2012; 3: 182.
  77. Beard E, Lengacher S, Dias S, Magistretti PJ, Finsterwald C. Astrocytes as Key Regulators of Brain Energy Metabolism: New Therapeutic Perspectives. Front Physiol. 2022; 12: 825816.
  78. De Keyser J, Mostert JP, Koch MW. Dysfunctional Astrocytes as Key Players in the Pathogenesis of Central Nervous System Disorders. J Neurol Sci. 2008; 267:  3-16.
  79. Bhattacharya   SK,   Muruganandam    AV.    Adaptogenic    activity of Withania somnifera: an experimental study using a rat model of chronic stress. Pharmacol Biochem Behav. 2003; 75: 547-555
  80. Nathan PJ, Clarke J, Lloyd J, Hutchison CW, Downey L, Stough C. The acute effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy normal subjects. Hum Psychopharmacol. 2001; 16: 345-351.
  81. Aguiar S, Borowski T. Neuropharmacological review of the nootropic herb Bacopa monnieri. Rejuvenation Res. 2013; 16: 313-326.
  82. Das AJ. Review on nutritional medicinal and pharmacological properties of Centella asiatica (Indian pennywort). J Biol Active Prod Nat. 2011; 1: 216-228.
  83. Chen S, Yin ZJ, Jiang C, Ma ZQ, Fu Q, Qu R, et al. Asiaticoside attenuates memory impairment induced by transient cerebral ischemia- reperfusion in mice through anti-infl ammatory mechanism. Pharmacol Biochem Behav. 2014; 122: 7-15.
  84. Lampariello LR, Cortelazzo A, Guerranti R, Sticozzi C, Valacchi G. The Magic Velvet Bean of Mucuna pruriens. J Tradit Complement Med. 2012; 2: 331-339.
  85. Ballantyne Jane C, Jianren Mao. Opioid Therapy For Chronic Pain. New England J Med. 2003; 349: 1943-1953.
  86. Ameri A. The effects of Aconitum alkaloids on the central nervous system. Progress in Neurobiology. 1998; 56: 211-235.
  87. Hou W, Wang Y, Zheng P, Cui R. Effects of Ginseng on Neurological Disorders. Front Cell Neurosci. 2020; 14: 55.
  88. Volgin AD, Yakovlev OA, Demin KA, Alekseeva PA, Kyzar EJ, Collins C, et al. “Understanding Central Nervous System Effects of Deliriant Hallucinogenic Drugs through Experimental Animal Models”. ACS Chemical Neuroscience. 2018.
  89. Malva JO, Santos S, Macedo T. Neuroprotective properties of Valeriana officinalis extracts. Neurotox Res. 2004; 6: 131-140.
  90. Yoshikawa T. Free radicals and their scavengers in Parkinson’s disease. Eur Neurol. 1994; 33: 60-68.
  91. Chahal AK, Chandan G, Kumar R, Chhillar AK, Saini AK, Saini RV. Bioactive constituents of Emblica officinalis overcome oxidative stress in mammalian cells by inhibiting hyperoxidation of peroxiredoxins. J Food Biochem. 2020; 44: e13115.
  92. Husain I, Zameer S, Madaan T, Minhaj A, Ahmad W, Iqubaal A, et al. Exploring the multifaceted neuroprotective actions of Emblica officinalis (Amla): a review. Metab Brain Dis. 2019; 34: 957-965.
  93. Mahendra P Bisht S. Ferula asafoetida: Traditional uses and pharmacological activity. Pharmacogn Rev. 2012; 6: 141-146.
  94. Alam W, Khan H, Khan SA, Nazir S, Akkol EK. Datura metel: A Review on Chemical Constituents Traditional Uses and Pharmacological Activities. Curr Pharm Des. 2021; 27: 2545-2557.
  95. Kennedy DO, Bonnländer B, Lang SC, Pischel I, Forster J, Khan J, et al. Acute and Chronic Effects of Green Oat (Avena sativa) Extract on Cognitive Function and Mood during a Laboratory Stressor in Healthy Adults: A Randomised Double-Blind Placebo-Controlled Study in Healthy Humans. Nutrients. 2020; 12: 1598.
  96. Sharma V, Sharma R, Gautam DS, Kuca K, Nepovimova E, Martins N. Role of Vacha (Acorus calamus Linn.) in Neurological and Metabolic Disorders: Evidence from Ethnopharmacology Phytochemistry Pharmacology and Clinical Study. J Clin Med. 2020; 9: 1176.
  97. Yadav MK, Singh SK, Singh M, Mishra SS, Singh AK, Tripathi JS, et al. Neuroprotective Activity of Evolvulus alsinoides & Centella asiatica Ethanolic Extracts in Scopolamine-Induced Amnesia in Swiss Albino Mice. Open Access Maced J Med Sci. 2019; 7: 1059-1066.
  98. Vallverdú-Queralt Anna, Regueiro Jorge, Martínez-Huélamo Miriam, Rinaldi Alvarenga José Fernando, Leal Leonel Neto, Lamuela-Raventos Rosa M. A comprehensive study on the phenolic profile of widely used culinary herbs and spices: Rosemary thyme oregano cinnamon cumin and bay”. Food Chemistry. 2014; 154: 299-307.
  99. Di Cesare Mannelli L, Micheli L, Maresca M, Cravatto G, Bellumori M, et al. Anti-neuropathic effects of Rosmarinus officinalis L. terpenoid fraction: relevance of nicotinic receptors. Sci Rep. 2016; 6: 34832.
  100. de Oliveira JR, Camargo SEA, de Oliveira LD. Rosmarinus officinalis L. (rosemary) as therapeutic and prophylactic agent. J Biomed Sci. 2019; 26.
  101. Bansal Y, Bansal G. Analytical methods for standardization of Aegle marmelos: A review. J Pharm Educ Res. 2011; 2: 37-44.
  102. Tandon PN. Indian Rauwolfia research led to the evolution of neuropsychopharmacology & the 2000 Nobel Prize (Part II). Indian J Med Res. 2021; 154: 169-174.

Gupta A, Pandey R, Singh S, Sharma B (2023) A Review on Toxins Mediated Neuro Diseases and Ameliorative Role of Certain Phytochemicals. J Pharmacol Clin Toxicol 11(3):1179.

Received : 06 Nov 2023
Accepted : 21 Dec 2023
Published : 23 Dec 2023
Annals of Otolaryngology and Rhinology
ISSN : 2379-948X
Launched : 2014
JSM Schizophrenia
Launched : 2016
Journal of Nausea
Launched : 2020
JSM Internal Medicine
Launched : 2016
JSM Hepatitis
Launched : 2016
JSM Oro Facial Surgeries
ISSN : 2578-3211
Launched : 2016
Journal of Human Nutrition and Food Science
ISSN : 2333-6706
Launched : 2013
JSM Regenerative Medicine and Bioengineering
ISSN : 2379-0490
Launched : 2013
JSM Spine
ISSN : 2578-3181
Launched : 2016
Archives of Palliative Care
ISSN : 2573-1165
Launched : 2016
JSM Nutritional Disorders
ISSN : 2578-3203
Launched : 2017
Annals of Neurodegenerative Disorders
ISSN : 2476-2032
Launched : 2016
Journal of Fever
ISSN : 2641-7782
Launched : 2017
JSM Bone Marrow Research
ISSN : 2578-3351
Launched : 2016
JSM Mathematics and Statistics
ISSN : 2578-3173
Launched : 2014
Journal of Autoimmunity and Research
ISSN : 2573-1173
Launched : 2014
JSM Arthritis
ISSN : 2475-9155
Launched : 2016
JSM Head and Neck Cancer-Cases and Reviews
ISSN : 2573-1610
Launched : 2016
JSM General Surgery Cases and Images
ISSN : 2573-1564
Launched : 2016
JSM Anatomy and Physiology
ISSN : 2573-1262
Launched : 2016
JSM Dental Surgery
ISSN : 2573-1548
Launched : 2016
Annals of Emergency Surgery
ISSN : 2573-1017
Launched : 2016
Annals of Mens Health and Wellness
ISSN : 2641-7707
Launched : 2017
Journal of Preventive Medicine and Health Care
ISSN : 2576-0084
Launched : 2018
Journal of Chronic Diseases and Management
ISSN : 2573-1300
Launched : 2016
Annals of Vaccines and Immunization
ISSN : 2378-9379
Launched : 2014
JSM Heart Surgery Cases and Images
ISSN : 2578-3157
Launched : 2016
Annals of Reproductive Medicine and Treatment
ISSN : 2573-1092
Launched : 2016
JSM Brain Science
ISSN : 2573-1289
Launched : 2016
JSM Biomarkers
ISSN : 2578-3815
Launched : 2014
JSM Biology
ISSN : 2475-9392
Launched : 2016
Archives of Stem Cell and Research
ISSN : 2578-3580
Launched : 2014
Annals of Clinical and Medical Microbiology
ISSN : 2578-3629
Launched : 2014
JSM Pediatric Surgery
ISSN : 2578-3149
Launched : 2017
Journal of Memory Disorder and Rehabilitation
ISSN : 2578-319X
Launched : 2016
JSM Tropical Medicine and Research
ISSN : 2578-3165
Launched : 2016
JSM Head and Face Medicine
ISSN : 2578-3793
Launched : 2016
JSM Cardiothoracic Surgery
ISSN : 2573-1297
Launched : 2016
JSM Bone and Joint Diseases
ISSN : 2578-3351
Launched : 2017
JSM Bioavailability and Bioequivalence
ISSN : 2641-7812
Launched : 2017
JSM Atherosclerosis
ISSN : 2573-1270
Launched : 2016
Journal of Genitourinary Disorders
ISSN : 2641-7790
Launched : 2017
Journal of Fractures and Sprains
ISSN : 2578-3831
Launched : 2016
Journal of Autism and Epilepsy
ISSN : 2641-7774
Launched : 2016
Annals of Marine Biology and Research
ISSN : 2573-105X
Launched : 2014
JSM Health Education & Primary Health Care
ISSN : 2578-3777
Launched : 2016
JSM Communication Disorders
ISSN : 2578-3807
Launched : 2016
Annals of Musculoskeletal Disorders
ISSN : 2578-3599
Launched : 2016
Annals of Virology and Research
ISSN : 2573-1122
Launched : 2014
JSM Renal Medicine
ISSN : 2573-1637
Launched : 2016
Journal of Muscle Health
ISSN : 2578-3823
Launched : 2016
JSM Genetics and Genomics
ISSN : 2334-1823
Launched : 2013
JSM Anxiety and Depression
ISSN : 2475-9139
Launched : 2016
Clinical Journal of Heart Diseases
ISSN : 2641-7766
Launched : 2016
Annals of Medicinal Chemistry and Research
ISSN : 2378-9336
Launched : 2014
JSM Pain and Management
ISSN : 2578-3378
Launched : 2016
JSM Women's Health
ISSN : 2578-3696
Launched : 2016
Clinical Research in HIV or AIDS
ISSN : 2374-0094
Launched : 2013
Journal of Endocrinology, Diabetes and Obesity
ISSN : 2333-6692
Launched : 2013
Journal of Substance Abuse and Alcoholism
ISSN : 2373-9363
Launched : 2013
JSM Neurosurgery and Spine
ISSN : 2373-9479
Launched : 2013
Journal of Liver and Clinical Research
ISSN : 2379-0830
Launched : 2014
Journal of Drug Design and Research
ISSN : 2379-089X
Launched : 2014
JSM Clinical Oncology and Research
ISSN : 2373-938X
Launched : 2013
JSM Bioinformatics, Genomics and Proteomics
ISSN : 2576-1102
Launched : 2014
JSM Chemistry
ISSN : 2334-1831
Launched : 2013
Journal of Trauma and Care
ISSN : 2573-1246
Launched : 2014
JSM Surgical Oncology and Research
ISSN : 2578-3688
Launched : 2016
Annals of Food Processing and Preservation
ISSN : 2573-1033
Launched : 2016
Journal of Radiology and Radiation Therapy
ISSN : 2333-7095
Launched : 2013
JSM Physical Medicine and Rehabilitation
ISSN : 2578-3572
Launched : 2016
Annals of Clinical Pathology
ISSN : 2373-9282
Launched : 2013
Annals of Cardiovascular Diseases
ISSN : 2641-7731
Launched : 2016
Journal of Behavior
ISSN : 2576-0076
Launched : 2016
Annals of Clinical and Experimental Metabolism
ISSN : 2572-2492
Launched : 2016
Clinical Research in Infectious Diseases
ISSN : 2379-0636
Launched : 2013
JSM Microbiology
ISSN : 2333-6455
Launched : 2013
Journal of Urology and Research
ISSN : 2379-951X
Launched : 2014
Journal of Family Medicine and Community Health
ISSN : 2379-0547
Launched : 2013
Annals of Pregnancy and Care
ISSN : 2578-336X
Launched : 2017
JSM Cell and Developmental Biology
ISSN : 2379-061X
Launched : 2013
Annals of Aquaculture and Research
ISSN : 2379-0881
Launched : 2014
Clinical Research in Pulmonology
ISSN : 2333-6625
Launched : 2013
Journal of Immunology and Clinical Research
ISSN : 2333-6714
Launched : 2013
Annals of Forensic Research and Analysis
ISSN : 2378-9476
Launched : 2014
JSM Biochemistry and Molecular Biology
ISSN : 2333-7109
Launched : 2013
Annals of Breast Cancer Research
ISSN : 2641-7685
Launched : 2016
Annals of Gerontology and Geriatric Research
ISSN : 2378-9409
Launched : 2014
Journal of Sleep Medicine and Disorders
ISSN : 2379-0822
Launched : 2014
JSM Burns and Trauma
ISSN : 2475-9406
Launched : 2016
Chemical Engineering and Process Techniques
ISSN : 2333-6633
Launched : 2013
Annals of Clinical Cytology and Pathology
ISSN : 2475-9430
Launched : 2014
JSM Allergy and Asthma
ISSN : 2573-1254
Launched : 2016
Journal of Neurological Disorders and Stroke
ISSN : 2334-2307
Launched : 2013
Annals of Sports Medicine and Research
ISSN : 2379-0571
Launched : 2014
JSM Sexual Medicine
ISSN : 2578-3718
Launched : 2016
Annals of Vascular Medicine and Research
ISSN : 2378-9344
Launched : 2014
JSM Biotechnology and Biomedical Engineering
ISSN : 2333-7117
Launched : 2013
Journal of Hematology and Transfusion
ISSN : 2333-6684
Launched : 2013
JSM Environmental Science and Ecology
ISSN : 2333-7141
Launched : 2013
Journal of Cardiology and Clinical Research
ISSN : 2333-6676
Launched : 2013
JSM Nanotechnology and Nanomedicine
ISSN : 2334-1815
Launched : 2013
Journal of Ear, Nose and Throat Disorders
ISSN : 2475-9473
Launched : 2016
JSM Ophthalmology
ISSN : 2333-6447
Launched : 2013
Annals of Psychiatry and Mental Health
ISSN : 2374-0124
Launched : 2013
Medical Journal of Obstetrics and Gynecology
ISSN : 2333-6439
Launched : 2013
Annals of Pediatrics and Child Health
ISSN : 2373-9312
Launched : 2013
JSM Clinical Pharmaceutics
ISSN : 2379-9498
Launched : 2014
JSM Foot and Ankle
ISSN : 2475-9112
Launched : 2016
JSM Alzheimer's Disease and Related Dementia
ISSN : 2378-9565
Launched : 2014
Journal of Addiction Medicine and Therapy
ISSN : 2333-665X
Launched : 2013
Journal of Veterinary Medicine and Research
ISSN : 2378-931X
Launched : 2013
Annals of Public Health and Research
ISSN : 2378-9328
Launched : 2014
Annals of Orthopedics and Rheumatology
ISSN : 2373-9290
Launched : 2013
Journal of Clinical Nephrology and Research
ISSN : 2379-0652
Launched : 2014
Annals of Community Medicine and Practice
ISSN : 2475-9465
Launched : 2014
Annals of Biometrics and Biostatistics
ISSN : 2374-0116
Launched : 2013
JSM Clinical Case Reports
ISSN : 2373-9819
Launched : 2013
Journal of Cancer Biology and Research
ISSN : 2373-9436
Launched : 2013
Journal of Surgery and Transplantation Science
ISSN : 2379-0911
Launched : 2013
Journal of Dermatology and Clinical Research
ISSN : 2373-9371
Launched : 2013
JSM Gastroenterology and Hepatology
ISSN : 2373-9487
Launched : 2013
Annals of Nursing and Practice
ISSN : 2379-9501
Launched : 2014
JSM Dentistry
ISSN : 2333-7133
Launched : 2013
Author Information X