Advancement of biomolecular engineering in Parkinson disease

Abstract

Parkinson's Condition (PD) is the second most common degenerative neurological disease, affecting 10 million people globally. Nigrostriatal degeneration is linked to decreased motor and non-motor functioning in this chronic illness. Resting tremor, stiffness, akinesia (or bradykinesia), and postural instability are the four cardinal symptoms of Parkinson's disease. Because the symptoms of Parkinson's disease are similar to those of other age-related disorders like SWEDD (scans without evidence of dopaminergic deficit), essential tremors, and Parkinson's disease, early diagnosis is difficult. A synucleinopathy is Parkinson's disease (PD) with Lewy Bodies (DLB).Although both genetic and environmental variables are assumed to play a role in Parkinson's disease (PD), there was no direct evidence to support either as a causal component until recently. Six distinct genes have been discovered as producing familial PD in the last eight years. They back up the idea that similar pathogenetic pathways exist across the spectrum of Parkinson's disease etiologies. Mutations in α-synuclein, parkin, UCHL1, DJ1, PINK1, and LRRK2 cause.Parkinson's disease, which is inherited in a Mendelian form. Overexpression of α- synuclein and parkin causes mitochondrial issues, but DJ1 and PINK1 are mitochondrial proteins. These same proteins regulate proteasomal function and play a role in the oxidative stress response.Doped carbon nanotubes, especially phosphorus-doped carbon nanotubes, can efficiently prevent the formation of α- synuclein amyloid, suggesting that they could be utilized to treat Parkinson's disease. More in vitro and clinical research is, however, necessary. As previously stated, αsynuclein could be a therapeutic target for Parkinson's disease and other synucleinopathies. The most promising option would be small chemicals that may modify the structure of protofibrillar forms of α-synuclein and render them nonpathogenic. Given the pathogenic consequences of αsynuclein's feed-forward amplification loops, a range of therapeutic options will almost certainly be required.