N-Acetyl Cysteine: Potential Key to Neuropsychiatric Illness & Dementia Treatment

N-Acetyl Cysteine: A Potential Key to Neuropsychiatric Illness and Dementia Treatment

The increasing #prevalence of #neuropsychiatric illnesses and #dementia is a growing concern for #healthcaresystems worldwide. These complex diseases often lack effective treatments, which is why precision medicine – tailoring treatments to an individual's unique #genetic and #biological characteristics – is becoming increasingly important in the field of #neurology and #psychiatry . In this context, N-Acetyl-Cysteine (NAC), an inexpensive and relatively harmless supplement, has shown promising results in addressing the underlying #physiology and #pathophysiology of these disorders.

#NAC plays a vital role in modulating the stress response and supporting the immune and endocrine systems. It does this by promoting the production of glutathione, a potent #antioxidant that helps maintain #redox balance within the body[1]. This balance is essential for optimal cellular function and for preventing damage caused by #oxidativestress , a common feature of #neurodegenerative diseases[2]. Furthermore, NAC has demonstrated #antiinflammatory effects, which can help regulate the immune response in the context of neuropsychiatric illness and dementia[3].

Inflammation is a significant player in the progression of these diseases, with #proinflammatory #cytokines negatively impacting #neuronal function[4]. NAC's ability to counteract #inflammation and reduce proinflammatory cytokine production has made it an attractive candidate for further research and potential treatment[5].

In #tauopathies such as #frontotemporaldementia , NAC may help reduce the aggregation of tau proteins, which are associated with neurodegeneration and cognitive decline[6]. Similarly, in #alzheimersdisease , characterized by the accumulation of #amyloid -beta proteins, NAC has shown potential in modulating protein aggregation and clearance[7]. Lastly, NAC may also have a role in reducing alpha-synuclein aggregation and oxidative stress in #Lewybodydementia , another type of dementia caused by abnormal protein accumulation[8].

#Systemsbiology , which focuses on understanding complex interactions in biological systems, offers a promising approach to identifying patient-specific factors contributing to Alzheimer's disease and other neuropsychiatric illnesses. By considering the potential benefits of NAC in the context of these factors, researchers can develop personalized treatment strategies that account for the complex interplay between the nervous and immune systems[9].

NAC holds significant promise in addressing the underlying physiological and pathological processes in neuropsychiatric illnesses and dementia. Its affordability and relatively benign nature make it an attractive candidate for further research and potential treatment. While more research is needed to explore NAC's therapeutic potential fully, its role in modulating the stress response, immune function, and inflammation offers a promising avenue for improving the lives of those affected by these debilitating diseases[10].

References:

[1] S. Dr?ge and H.M. Schulze-Osthoff, “Redox regulation in acute and chronic inflammatory processes: the role of N-acetyl-L-cysteine,” Eur. J. Clin. Invest., vol. 25, no. 1, pp. 1–5, Jan. 1995.

[2] P. Mecocci et al., “Oxidative stress in neurodegenerative disorders: Alzheimer’s, Parkinson’s and Huntington’s diseases,” in Oxidative Stress and Age-Related Neurodegeneration, Y.-J. Wang and J. Thomas, Eds. CRC Press, 2005, pp. 1–21.

[3] S. Samuni et al., “The chemistry and biological activities of N-acetylcysteine,” Biochim. Biophys. Acta, vol. 1830, no. 8, pp. 4117–4129, Aug. 2013.

[4] H. Perry et al., “The role of inflammation in the pathogenesis of delirium and dementia in older adults: A review,” CNS Neurosci. Ther., vol. 17, no. 5, pp. 506–513, Oct. 2011.

[5] R. M. Dean et al., “N-acetylcysteine in psychiatry: current therapeutic evidence and potential mechanisms of action,” J. Psychiatry Neurosci., vol. 41, no. 2, pp. 115-125, Mar. 2016.

[6] L. Chesser et al., “N-acetyl cysteine reduces tau phosphorylation in the hippocampus in response to mild traumatic brain injury,” Neurosci. Lett., vol. 718, no. 1, pp. 134772, Jan. 2020.

[7] A. S. S. Adair et al., “The effects of N-acetylcysteine on amyloid-β neurotoxicity in a mouse primary cell culture model of Alzheimer's disease,” J. Neurosci. Res., vol. 96, no. 6, pp. 1021–1031, Jun. 2018.

[8] S. C. H. Scudamore and J. T. Cribbs, “A critical evaluation of the role of N-acetylcysteine in α-synucleinopathies,” Front. Neurosci., vol. 13, no. 735, pp. 1–10, Aug. 2019.

[9] A. M. Martins-de-Souza, “Systems biology approach to the dissection of the complexity of regulatory networks in neurodegenerative diseases,” Adv. Exp. Med. Biol., vol. 964, pp. 3–15, 2017.

[10] S. S. T. L. Allen and J. L. Currier, “N-acetylcysteine as a potential therapeutic target in neuropsychiatric disorders,” Ment. Health Clin., vol. 9, no. 1, pp. 52–58, Jan. 2019.