Nsgene expression from adenoviral vector in regions like thalamus and striatum. Employing human cytomegalovirus (CMV) enhancer and platelet-derived growth element B-chain (PDGF-), a neuron-specific promoter, neuronal transgene expression can be enhanced and this can be useful in the study of gene therapy in case of neurological problems. Cytomegalovirus enhancer and SYN promoter with LV as vector showed persistent neuronal expression. Phosphate-activated glutaminase (PAG) as well as vesicular glutamate transporter-1 (VGLUT1) promoters incorporated into herpesvirus can express glutamatergic neurons, whereas glutamic acid decarboxylase-67 (GAD67) promoter driven by herpesvirus supports expression of GABAergic neuron. Nigrostriatal neuron-specific expression by GDNF or BDNF from herpes simplex virusvectors are beneficial for investigating gene therapy of Parkinson’s diseases [122]. Promoters in AD Human PAD gene are promoter of A4 amyloid protein and has close resemblance with that of housekeeping genes possessing 72 GC-rich content within the DNA area. PAD gene regulation is often achieved according to four mechanisms, the GC-rich element involved possible protein binding, CpG area methylation, AP-1/Fos binding site associated with oncogene, along with the stress-related heat shock manage element [127]. A study by Ohyagi et al. demonstrated the activation of p53 promoter by particular binding of A42 causing possibilities of p53-dependent neuronal apoptosis, synaptic degeneration, mitochondrial dysfunction involved in AD [128]. An Italian case ontrol study by Bizzarro et al. on APOE promoter interaction in AD confirmed genetic danger components especially for ACG3, ATT4, and ATG4 haplotypes, and single-nucleotide polymorphisms (SNP) in APOE promoter gene is often independent of 4 risk elements [129]. An additional study reports a weak association of APOC1 promoter ROCK1 Formulation polymorphism in AD [130]. An additional association is the polymorphism in PIN1 promoter at – 842 (G C) and – 667 (C T) regions to have an elevated danger of AD [131]. Myeloperoxidase (MPO) gene promoter polymorphism in Chinese Han population has also been reported to have a contribution in AD risk by way of MPO regulation [132]. Promoters in PD Based on hypothesis and unbiased (derived from a microarray study) approach, Wettergren et al. made efforts for choice and evaluation of promoter candidates relevant for PD that might prove valuable for the illness therapy using gene therapy approaches. Prodynorphin (pDyn), dopamine receptor 1a (Drd1a), and dopamine receptor two (Drd2) had been selected according to hypothesis method. From a microarray study angiotensin I converting enzyme (ACE), DnaJ (Hsp40) homolog, microtubule-associated protein 1A (MAP1A), N-Acetylgalactosamine-6-sulfatase (GALNS), and ring finger protein 25 (RNF25) were selected based on unbiased approach. All candidates chosen determined by each ACAT1 drug approaches showed far more than 90 neuronal specificity and have been in a position to express transgene in rat striatum however the ones selected from microarray study showed highest efficacy [133]. One more study conducted on Prkd1 gene promoter characterization MN9D dopaminergic neuronal cells showed PKD1 to have a neuroprotective role in dopaminergic neurons in the course of oxidative anxiety at early stages and may possibly contribute to PD drug improvement [134]. Neuron-specific T1 -tubulin (T1) promoter induced neuronal-specific expression of Gli1 showed neuroprotective activity. Suwelack et al. concludesMolecular Neurobiology (2022) 59:191that neuro.
