INTRODUCTION:

One of the most significant first-line medications for treating tuberculosis is Isoniazid (Isonicotinic acid hydrazide or INH), a synthetic antibiotic. The medication has been at the forefront of antituberculosis treatment since its introduction in 1952, mostly because of its great selectivity and potency against Mycobacterium tuberculosis¹. The catalase-peroxidase KatG activates Isoniazid, a prodrug that produces a range of radicals and adducts that prevent the mycobacterium from producing the mycolic acids that make up its cell wall. Because of its activity, Isoniazid has the potential to be a powerful bactericidal agent. Additionally, the medication seems to work in concert with other KatG-produced species and other TB treatments.^2,3

Isoniazid (INH) has recently attracted scientific attention due to its possible therapeutic value in neurodegenerative diseases. Emerging experimental evidence indicates that Isoniazid and its chemically modified derivatives may provide important neuroprotective effects, despite the fact that its typical clinical use is not in neurology. The straightforward chemical structure of Isoniazid offers a great framework for creating novel compounds with anti-inflammatory, anti-apoptotic, and antioxidant qualities—mechanisms that are essential for delaying the onset of illnesses like Parkinson's, Alzheimer's, and Huntington's disease Mechanistically, Isoniazid suppressed monoamine oxidase B (MAO-B) and BACE1 (β-site amyloid precursor protein cleaving enzyme 1), both of which are linked to amyloid pathology. Additionally, Isoniazid reduced the activation of astrocytes and microglia surrounding amyloid plaques, indicating anti-inflammatory effects in the brain.^4,5.In preclinical models, a number of Isoniazid-based compounds have shown encouraging action in lowering protein aggregation, maintaining mitochondrial function, and promoting neuronal survival. Furthermore, some derivatives may have therapeutic utility for Parkinson's disease via modulating dopaminergic pathways. Clinical research from the past indicates that Isoniazid decreased levodopa-induced dyskinesias in Parkinson's patients, even at the expense of exacerbating parkinsonian symptoms. This implies that Isoniazid's relationship with dopamine signaling is complicated and although it may modulate dopamine systems or lessen the negative effects of dopaminergic medication.^6,7 With its effectiveness against Isoniazid-resistant Mycobacterium tuberculosis, minimal cytotoxicity, and favorable pharmacokinetic characteristics, this novel isoniazid derivative for tuberculosis molecule may serve as a foundation for future medicinal chemistry designed for both TB and CNS applications.⁸ Antioxidant Derivatives: Isoniazid derivatives were synthesized and reacted with several aldehydes in a 2024 study; some of these compounds demonstrated DPPH radical scavenging activity, which is a surrogate for antioxidant capability.⁹ These results demonstrate the growing interest in altering or utilizing isoniazid to create new, focused therapies for neurodegenerative diseases.

Structure and properties:

Fig(1)- Isoniazid molecular and 3D structure

Physical and chemical properties of Isoniazid:

Table 1:Properties of isoniazid¹⁰

Property	Description
Appearance	Colourless or white crystalline powder
Odour	Odourless
Taste	Slightly sweet at first, followed by a bitter aftertaste
Melting Point	171°C
pH (1% aqueous solution)	5.5 – 6.5
Solubility	Soluble in both water and organic solvents
Polarity	Negative LogP value of -0.64, indicating the compound is more polar than non-polar
Acidity/Basicity	Slightly acidic in nature (pH 5.5–6.5 for a 1% aqueous solution)

Neurodegenerative Disorder:

Neurodegenerative disorders are characterized by the purposeful loss of neurons, which usually results in death. Progressive neuropsychiatric illnesses include Alzheimer's disease, Multiple sclerosis, Parkinson's disorder, Amyotrophic lateral sclerosis, Huntington's disease, and a variety of other neurodegenerative disorders¹¹. Neurodegenerative disorders preferentially affect different areas of the brain (e.g., frontotemporal cortex, basal ganglia, spinocerebellar tracts, or spinal motor neurons) causing different patterns of neurological deficits (e.g., dementia, parkinsonism, ataxia, or muscular weakness).¹² One perplexing aspect is that some neuronal populations—such as dopaminergic neurons in the substantia nigra in Parkinson's disorders and medium spiny neurons in Huntington's disease—are disproportionately impacted even though many neurons share the same breakdown processes.¹³ Furthermore, illness frequently starts in a specific area of the brain and subsequently "spreads" through interconnected networks or the extracellular spread of harmful proteins.¹⁴ Despite having similar molecular themes, different neurodegenerative disorders exhibit unique anatomical-clinical patterns, which can be explained by this selective vulnerability plus network propagation. The majority of neurodegenerative disorders now have symptomatic rather than disease-modifying therapy options. For instance, riluzole in ALS, L-DOPA in Parkinson's disease, and cholinesterase inhibitors in Alzheimer's disorders mostly impede rather than reverse damage.¹⁵ Reaching susceptible neurons after substantial degeneration has already taken place is challenging due to the multifactorial nature of disorder (several mechanisms operating simultaneously). Targeting upstream pathways (protein aggregation, mitochondrial support, neuroinflammation) or encouraging neuronal regeneration and resilience are the goals of some new treatments.¹¹ A major global public health concern, particularly as populations age, is neurodegenerative illnesses. Patients, caregivers, and healthcare systems are severely burdened by them. For instance, Parkinson's disorder is one of the neurological conditions with the quickest rate of growth, while Alzheimer's disorder is the most frequent cause of dementia.¹⁶ Neurodegenerative disorders are shown in Fig(2).

Fig(2).Neurodegenerative disorders

Mechanism of Neurodegenerative Disorders:

Numerous interrelated processes that progressively harm neurons lead to the development of neurodegenerative disorders. One important cause is the build-up of misfolded proteins that interfere with normal cellular functions, such as tau and amyloid-β in Alzheimer's disorders or α-synuclein in Parkinson's disorders¹⁷. Oxidative stress and cellular damage result from mitochondrial malfunction, which lowers energy production and raises reactive oxygen species. Neuronal degeneration is further exacerbated by chronic neuroinflammation, which is fueled by activated microglia and compromised astrocytes¹⁸. Toxic proteins accumulate in cells due to impairment of protein clearance systems, such as the ubiquitin–proteasome and autophagy–lysosome pathways; excitotoxicity brought on by excessive glutamate activity raises intracellular calcium levels, which initiates cell death pathways; synaptic dysfunction and impaired axonal transport impair neuronal communication; genetic mutations can exacerbate these pathological changes; all of these mechanisms combine to produce a cycle of progressive cellular damage that eventually results in neurodegenerative disorders^19,20. The mechanism of neurodegenerative disease is shown in Fig(3).

Fig (3). General cause of neurodegenerative disorders

Global Burden and Future Projection of Neurodegenerative Disorders (2025) Status and Beyond:

Graph 1: Percentage of total Global Neurodegenerative Cases in 2025

The World Health Organization (WHO) estimates that there were approximately 57 million dementia sufferers worldwide in 2021, with more than 60% living in low- and middle-income nations. According to a recent 2025 estimate, the expanding older-adult population was a major factor in the ≈ 1.6-fold increase in the global frequency of Alzheimer's disorders and other dementias among individuals 65 and older between 1991 and 202²¹. The global burden of neurodegenerative illnesses, primarily dementia/AD and Parkinson's disorders (PD), is increasing in terms of disability-adjusted life years, or DALYs. An assessment conducted in 2024 discovered current burdens and forecasted additional rises through 2050. Based on the 2021 Global Burden of Disease Study (GBD 2021), a global study on Parkinson's disease finds increasing prevalence and forecasts future burden from 2022 to 2035 using statistical modeling.^22. According to a 2025 projection study, the prevalence of Parkinson's disorders (PD) is expected to reach ≈ 267 cases per 100,000 persons by 2050, a significant increase from 2021 and highlighting a sharp development trend over the ensuing decades²³. The global burden and future projection of neurodegenerative disorders is given in the above graph.

Isoniazid Anti-Bacterial Activity:

Fig(4)Anti- bacterial activity of isoniazid moieties

Hydrazide and Pyridine:

Isoniazid's isonicotinyl hydrazide moiety, which is activated by the Mycobacterium TB enzyme KatG, is principally responsible for its antibacterial activity^[24].The hydrazide moiety inhibits InhA, a crucial enzyme in the formation of mycolic acid, a crucial part of the mycobacterial cell wall, by forming a reactive isonicotinyl–NAD+ adduct upon activation²⁵. This inhibition prevents the production of protective mycolic acids, which disrupts the integrity of the bacterialcell wall and eventually results in bacterial cell death ^[26]. The hydrazide group is the essential component that gives the medication its antimycobacterial activity, however the pyridine ring aids in the correct binding and stabilization of this active adduct^27,28. Role of hydrazide and pyridine moieties of isoniazid in anti-bacterial activity is shown in Fig(4).

Isoniazid in neurodegenerative disorders:

Table2: Isoniazid role in some neurodegenerative disorders^{33,34,35,36,37}

S. No	Neurodegenerative disease	Alzheimer’s disease (AD)	Parkinson’s disease (PD)	Huntington’s disease (HD)	Amyotrophic lateral sclerosis (ALS)	Frontotemporal dementia (FTD) / other tauopathies
1	Major Pathophysiology (short)	Amyloid-β aggregation, tau illness, neuroinflammation, and synaptic loss.	Lewy bodies (α-synuclein) and progressive loss of dopaminergic neurons in the substantia nigra.	CAG repeat → mutant hunting leading to loss of neurons, particularly in the striatum → chorea, dementia.	oxidative stress, neuroinflammation, glutamate excitotoxicity, and degeneration of both upper and lower motor neurons.	Behavioral and linguistic disorders; tau or TDP-43 proteinopathy; loss of frontotemporal cortical neurons.
2	Key Neuro-transmitter affected	A significant loss of cholinergic (ACh) and glutamate excitotoxicity	Dopamine (DA).	Glutamate circuits and GABA (striatal medium spiny neurons).	Glutamate (excitotoxicity); impact on several systems.	Several (including glutamatergic and cholinergic).
3	Proposed Mechanism(s) of Isoniazid (INH) relevant to disease	It has been suggested that INH (and some of its derivatives) can lower the burden of Aβ, control neuroinflammation, and function as a multi-target small molecule (metal chelation, antioxidant action demonstrated for certain derivatives).	Mixed and indirect methods have been proposed: INH can interfere with pyridoxal-5'-phosphate-dependent pathways that regulate GABA/glutamate and, consequently, motor circuitry; it has also been shown to change levodopa-induced dyskinesias (perhaps by changing GABAergic balance or drug interactions).	Hypothetical relevance: INH would be predicted to worsen rather than alleviate GABAergic deficiencies since it lowers GABA production by causing pyridoxine (B6) antagonism. Benefit is not supported by strong preclinical or clinical evidence; some molecular reasoning points to a worsening risk.	There is no obvious connection between INH and the preservation of motor neurons. The recognized actions of INH (pyridoxine interaction, potential oxidative effects) do not offer a neuroprotective explanation for ALS; some INH compounds with antioxidant characteristics have been investigated in neurodegenerative concepts, but they are not ALS-specific.	INH has no disease-specific data. It is unknown if the effects of INH on amyloid pathology and local inflammation in the AD mice model translate into tauopathies.
4	Current Standard Drugs / Classes	AChE inhibitors (donepezil, rivastigmine), memantine	Levodopa ± dopa-decarboxylase inhibitors, dopamine agonists, MAO-B inhibitors, COMT inhibitors	Tetrabenazine/deutetrabenazine (for chorea); symptomatic care	Riluzole, edaravone (modest effects); supportive care	Supportive/symptomatic; no disease-modifying drugs approved for most FTDs
5	Experimental / clinical outcome (summary)	Oral INH preserved dendritic synapses, decreased Aβ plaques and local innate immune cells, and enhanced cognition in APP/PS1 mouse models. These are encouraging preclinical findings, although they are currently restricted to animal models.	short clinical observations/trials: a short open/controlled series found that INH reduced levodopa-induced dyskinesia in certain patients; other reports indicate that patients on anti-TB regimens may experience medication interactions or exacerbation of parkinsonism (thus effects are vary). not recognized as a form of therapy.	There is no solid experimental or clinical proof that INH improves HD; however, there is theoretical worry that B6 antagonism may exacerbate GABA-related symptoms.	There is no preclinical or clinical evidence to support INH in ALS; animal research suggests caution due to the possibility of neurotoxicity at high INH doses.	There is just mechanistic extrapolation and no experimental or clinical data to support the use of INH in FTD.

Approximately 75% of the conceptual research now being conducted on isoniazid (INH) in neurodegenerative illnesses is devoted to Alzheimer's disease. At about 20%, Parkinson's disease accounts for a smaller but significant portion of the research focus, whereas other neurodegenerative diseases like multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS) receive little attention and only account for 5%.

Fig(5). Graphical representation of isoniazid utilization in neurodegenerative disorders

Isoniazid in Parkinson:

Due to its distinct chemical structure and neuropharmacological effects, isoniazid (INH), despite being predominantly an anti-tubercular medication, has demonstrated experimental advantages in Parkinson's disorder (PD). Isoniazid may indirectly improve dopaminergic neurotransmission, which is lacking in Parkinson's disorder (PD), according to research ³⁸. In experimental Parkinson disorder models, isoniazid may assist restore motor balance and alleviate bradykinesia and rigidity by lowering excessive GABAergic inhibition in the basal ganglia circuitry.

Furthermore, the aromatic isonicotinyl ring helps lessen dopamine breakdown by contributing to modest monoamine oxidase-B (MAO-B) inhibitory actions³⁹. This activity is mostly caused by the hydrazide moiety (-CONHNH₂) in isoniazid⁴⁰. Pyridoxal-5-phosphate (vitamin B6) and this hydrazide group combine to generate a Schiff base, which momentarily inhibits pyridoxine-dependent enzymes involved in GABA production ⁴¹. However, its structure offers insight for the development of novel hydrazide-based neuroprotective medicines. Isoniazid role in inhibition of Parkinson disease is shown in fig(6).

Fig(6). Mechanism of Isoniazid in Parkinson’s disorder

Relationship between Hydrazide and Neurodegenerative Disease:

Acetylcholinesterase (AChE) inhibition is used to treat AD symptoms. At micromolar (often low-to-mid μM) doses, numerous hydrazide/hydrazone compounds inhibit AChE in vitro; the hydrazone linkage offers H-bonding interactions and places aromatic groups into the cholinesterase active-site gorge. Dual-site AChE ligands (catalytic + peripheral sites) have been proposed for the hydrazone/hydrazide series⁴¹. The multi-target directed ligand (MTDL) strategy was supported by some isoniazid-derived acylhydrazones that were specifically screened for MPO inhibition (MPO contributes to oxidative neuroinflammation) and demonstrated activity in biochemical testing. Hydrazide leads to the acylhydrazone transformation: adding various acyl fragments (aryl, heteroaryl, chelators) to the hydrazide results in acylhydrazones that incorporate metal-binding motifs, adjust lipophilicity, and have the capacity to pass the blood-brain barrier. This is the most popular method for converting (GABA) in multiple INH into multi-target AD leads.^40. The experiment was founded on the discovery that HD is linked to a deficit of the inhibitory neurotransmitter gamma-aminobutyric acid brain areas. It has been established that isoniazid (INH) inhibits GABA aminotransferase (GABA-T), an enzyme that breaks down GABA. High dosages of INH were thought to boost GABA levels in the brain, relieving in HD patients' symptoms. A preliminary open trial had already indicated a potential benefit for certain patients.⁴²

CONCLUSION:

Traditionally regarded as a powerful first-line anti-tuberculosis medication, isoniazid (INH) is becoming more widely acknowledged for its wider therapeutic value, especially in neurodegenerative illnesses. Its hydrazide and pyridine moieties facilitate a variety of metabolic interactions, such as antioxidant activity, pyridoxal-5-phosphate-dependent pathway regulation, MAO-B inhibition, and neuroinflammation attenuation. Numerous clinical characteristics of Alzheimer's, Parkinson's, Huntington's disease, and associated illnesses are consistent with these pathways. Preclinical research shows that INH and its derivatives decrease activated glial cells, protect mitochondria, maintain synaptic architecture, and lessen the load of amyloid. The potential of INH to lessen levodopa-induced dyskinesias in Parkinson's disease shows complicated neuromodulatory effects due to its action on dopaminergic and GABAergic pathways. The molecule is a promising framework for the creation of multi-target drugs due to its chemical simplicity, modifiability, and low toxicity profile, despite the fact that clinical evidence is still few and occasionally inconsistent. All things considered, INH has great promise as a basis for cutting-edge neuroprotective treatments that target various disease processes.

REFERENCE:

1. Fernandes GFDS, Salgado HRN, Santos JLDS. Isoniazid: a review of characteristics, properties and analytical methods. 2017 Jul 4; 47(4): 298–308.

2. O'Connor C, Patel P, Brady MF. Isoniazid. Treasure Island (FL): StatPearls Publishing; 2025 Jan.

3. Joydeep P, Nasiruddi M, Ahmad KI, Ali KR, Hasan AS. Therapeutic effect of Nigella sativa oil in hepatotoxicity induced by isoniazid in rats. Apr–Jun 2019; 53(2).

4. Jishnu S, Anjali C, Ramandeep S, Dinesh M. Isoniazid-historical development, metabolism associated toxicity and a perspective on its pharmacological improvement, 2024 Sep 19: 15: 1441147.

5. Chen J, Guo N, Ruan Y, Mai Y, Liao W, Feng Y. Isoniazid improves cognitive performance, clears Aβ plaques, and protects dendritic synapses in APP/PS1 transgenic mice. 2023 Jan 19; 15:1105095. Perry TL, Wright JM, Hansen S, Thomas SMB, Allan BM, Baird PA. A double-blind clinical trial of isoniazid in Huntington disease. April 1982; 32(4):354.

6. Gershanik OS, Luquin MR, Scipioni O, Obeso JA. Isoniazid therapy in Parkinson's disease. 1988;3(2):133–9.

7. Santos DC, Henriques RR, Lopes Junior MAA, Farias AB, Nogueira TLC, Quimas JVF. Acylhydrazones as isoniazid derivatives with multi-target profiles for the treatment of Alzheimer's disease: radical scavenging, myeloperoxidase/ acetylcholinesterase inhibition and biometal chelation. 2020 May 15; 28(10): 115470.

8. Volynets GP, Tukalo MA, Bdzhola VG, Derkach NM, Gumeniuk MI, Tarnavskiy SS, Yarmoluk SM. Novel isoniazid derivative as promising antituberculosis agent. 2020 Jul; 15(10):869–879.

9. Gadhave DG, Sugandhi VV, Jha SK, Nangare SN, Gupta G, Singh SK. Neurodegenerative disorders: mechanisms of degeneration and therapeutic approaches with their clinical relevance. 2024; 99: 102357.

10. Ghosh S. Breathing disorders in neurodegenerative diseases. 2022; 189:223–239.

11. Muddapu VR, Dharshini SAP, Chakravarthy VS, Gromiha MM. Neurodegenerative disorders - is metabolic deficiency the root cause? 2020; 31: 14:213.

12. Davenport F, Gallacher J, Kourtzi Z, Koychev I, Matthews PM, Oxtoby NP. Neurodegenerative disease of the brain: a survey of interdisciplinary approaches. 2023 Jan; 20(198): 20220406.

13. Kharat S, Mali S, Korade G, Gaykar R. Navigating neurodegenerative disorders: a comprehensive review of current and emerging therapies for neurodegenerative disorders. 2024;8(1)

14. Lamptey RNL, Chaulagai B, Trivedi R, Gothwal A, Layek B, Singh J. A review of the commen neurodegenerative disorder: current therapeutic approaches and the potential role of nanotherapeutics. 2022; 23(3): 1851.

15. Toader C, Tataru CP, Munteanu O, Serban M, Covache-Busuioc RA, Ciurea AV. Decoding neurodegeneration: a review of molecular mechanisms and therapeutic advances in Alzheimer’s, Parkinson’s, and ALS. 2024; 25(23): 12613.

16. Koszła O, Sobek P. Misfolding and aggregation in neurodegenerative diseases: protein quality control machinery as potential therapeutic clearance pathways. 2024.

17. Lin MT, Beal MF. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature. 2006;443(7113):787–795.

18. Nixon RA. The role of autophagy in neurodegenerative disease. Nat Med. 2013; 19(8): 983–997.

19. Singleton AB, Hardy J. The evolution of genetics: Alzheimer’s and Parkinson’s diseases. Neuron. 2016; 90(6): 1154–1163.

20. Wilson DM, Cookson MR, Bosch VDL, Zetterberg H, Holtzman DM, Dewachter I. Hallmarks of neurodegenerative diseases. 2023; 186(4): 693–714.

21. Chao G, Jingwen J, Yuyan T, Shengdi C. Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets, 2023 sep 22; 8(1):359

22. Zhu X, Yu J, Lai X, Wang X, Deng J, Long Y. Global burden of Alzheimer's disease and other dementias in adults aged 65 years and older, 1991–2021: population-based study. 2025 Jul 1; 13: 1585711.

23. Wang S, Jiang Y, Yang A, Meng F, Zhang J. The expanding burden of neurodegenerative diseases: an unmet medical and social need. 2024 Nov 4;16(5):2937–2952.

24. Luo Y, Qiao L, Li M, Wen X, Zhang W, Li X. Global, regional, national epidemiology and trends of Parkinson's disease from 1990 to 2021: findings from the Global Burden of Disease Study 2021. 2025 Jan 10; 16:1498756.

25. Su D, Cui Y, He C, Yin P, Bai R, Zhu J. Projections for prevalence of Parkinson's disease and its driving factors in 195 countries and territories to 2050: modelling study of Global Burden of Disease Study 2021. 2025 Mar 5;388: e080952.

26. Wei CJ, Lei B, Musser JM, Tu S-C. Isoniazid activation defects in recombinant Mycobacterium tuberculosis catalase-peroxidase (KatG) mutants evident in InhA inhibitor production. 2003 Feb;47(2):670–675.

27. Argyrou A, Vetting MW, Blanchard JS. New insight into the mechanism of action of and resistance to isoniazid. 2007 Jul 18;129(31):9582–9583.

28. Vilchèze C, Jacobs WR Jr. The mechanism of isoniazid killing: clarity through the scope of genetics. 2007; 61:35–50.

29. Timmins GS, Deretic V. Mechanisms of action of isoniazid. 2006 Dec;62(5):1220–7.

30. Brunton. L.L, Chabner. B.A, Knollmann. B.C. Goodman and Gilman’s The Pharmacological Basis of Therapeutics.

31. Pahlavani E, Kargar H, Sepehri Rad N. A study on antitubercular and antimicrobial activity of isoniazid derivative. 2015;17(7).

32. Badrinath M, Chen RJ, John S. Isoniazid toxicity. Treasure Island (FL): StatPearls; 2025 Jan.

33. Çelik H, Kucukler S, Çomaklı S, Caglayan C, Özdemir S, Yardım A. Neuroprotective effect of chrysin on isoniazid-induced neurotoxicity via suppression of oxidative stress, inflammation and apoptosis in rats. Neurotoxicology. 2020 Dec; 81:197–208.

34. Chen J, Guo N, Ruan Y, Mai Y, Liao W, Feng Y. Isoniazid improves cognitive performance, clears Aβ plaques, and protects dendritic synapses in APP/PS1 transgenic mice. Front Aging Neurosci. 2023 Jan 19;15:Article 1105095.

35. Hallett M, Lindsey JW, Adelstein BD, Riley PO. Controlled trial of isoniazid therapy for severe postural cerebellar tremor in multiple sclerosis. 1985 Sep;35(9):1374.

36. Bartolić M, Matošević A, Maraković N, Bušić V, Roca S, Vikić-Topić D. Evaluation of hydrazone and N-acylhydrazone derivatives of vitamin B6 and pyridine-4-carbaldehyde as potential drugs against Alzheimer’s disease. J Enzyme Inhib Med Chem. 2024;39(1).

37. Gershanik OS, Luquin MR, Scipioni O, Obeso JA. Isoniazid therapy in Parkinson's disease. Mov Disord. 1988;3(2):133–9.

38. Sekar PKC, Thomas SM. An overview of the role of monoamine oxidase-B in Parkinson’s disease: implications for neurodegeneration and therapy. Explor Neuroprot Ther. 2024; 4:308–318.

39. Peedikayil AT, Lee J, Abdelgawad MA, Ghoneim M, Shaker ME, Selim S, Kumar S. Inhibitions of monoamine oxidases by ferulic acid hydrazide derivatives: synthesis, biochemistry, and computational evaluation. Appl Biol Chem. 2023 Oct 5.

40. Santos DC, Henriques RR, Lopes Junior MAA, Farias AB, Nogueira TLC, Quimas JVF. Acylhydrazones as isoniazid derivatives with multi-target profiles for the treatment of Alzheimer’s disease: radical scavenging, myeloperoxidase/acetylcholinesterase inhibition and biometal chelation. Bioorg Med Chem. 2020 May 15;28(10):115470.

41. Iraji A, Nikfar P, Montazer MN, Karimi M, Edraki N, Saeedi M, Mirfazli SS. Synthesis, biological evaluation and molecular modeling studies of methyl indole-isoxazole carbohydrazide derivatives as multi-target anti-Alzheimer’s agents. 10 September 2024.

42. Perry TL, Wright JM, Hansen S, MacLeod PM. Isoniazid therapy of Huntington disease. 1979 Mar; 29(3):370-5.

Received on 22.01.2026 Revised on 23.02.2026

Accepted on 24.03.2026 Published on 22.04.2026

Available online from April 24, 2026

Res.J. Pharmacology and Pharmacodynamics.2026;18(2):205-211.

DOI: 10.52711/2321-5836.2026.00028

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