The therapeutic potential of heterocyclic compounds in neurodegenerative illnesses such as Alzheimer's and Parkinson's has garnered a lot of attention. These molecules target signaling pathways and mitochondrial homeostasis. Although the exact processes that cause Parkinson's disease and promotion are still unknown, there is a lot of evidence that a faulty cell reinforcement system, mitochondrial dysfunction, intracellular Ca2+ dyshomeostasis, and an excess of (ROS and RNS) all play important roles in the pathophysiology of these neurological disorders. Technological progress in the future has led to a dramatic increase in the prevalence of neurological diseases associated with aging. However, except from severely limited palliative care, there is no effective defensive treatment or treatment available. Consequently, there is an immediate need to enhance disease-modifying treatments and preventative measures to address Promotion/PD. A neuroprotective pathway for treating neurodegenerative illnesses may be shown by differentiating evidence or the development of drugs suitable for reestablishing Ca2+ homeostasis and signaling, since dysregulated Ca2+ metabolism promotes oxidative damage and neuropathology in these conditions. Decreased Ca2+ take-up through voltage-operated Ca2+ channels (VOCCs) is one of several methods to regulate mitochondrial Ca2+ homeostasis and signaling. Several heterocyclic compounds have modulatory effects on Ca2+ homeostasis and dealing, and this article surveys those effects. It also discusses how these compounds can direct impaired mitochondrial capability and related free-revolutionary production in the beginning and development of Parkinson's disease (PD). In addition to summarizing the clinical preliminary results, this thorough audit details the heterocycles' substance synthesis.