Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Nano-Theranostics Approaches and Mitochondrial Targeted Drug Delivery: Alzheimer ’s Disease Therapeutic Interventions

Version 1 : Received: 31 October 2022 / Approved: 1 November 2022 / Online: 1 November 2022 (14:29:26 CET)

How to cite: Chacko, L.; Nag, S.; Dewanjee, S.; Ghosh, S.; Vallamkondu, J.; Mitra, O.; Dey, A.; Bhuniya, T.; Paluru, H.P.R.; Reddy, P.H.; Kandimalla, R. Nano-Theranostics Approaches and Mitochondrial Targeted Drug Delivery: Alzheimer ’s Disease Therapeutic Interventions. Preprints 2022, 2022110032. https://doi.org/10.20944/preprints202211.0032.v1 Chacko, L.; Nag, S.; Dewanjee, S.; Ghosh, S.; Vallamkondu, J.; Mitra, O.; Dey, A.; Bhuniya, T.; Paluru, H.P.R.; Reddy, P.H.; Kandimalla, R. Nano-Theranostics Approaches and Mitochondrial Targeted Drug Delivery: Alzheimer ’s Disease Therapeutic Interventions. Preprints 2022, 2022110032. https://doi.org/10.20944/preprints202211.0032.v1

Abstract

One of the most frequent brain diseases, Alzheimer's is defined by poor cognitive function brought on by the build-up of Beta Amyloid plaques and the gradual death of neurons. Glucose metabolism and the development of amyloid plaques are being studied together. Under physiologically normal circumstances, glucose is the primary substrate for the adult human brain. The prodromal phases of AD are significantly influenced by glucose hypometabolism. Hypometabolism of glucose in the brain is a clear sign of mitochondrial dysfunction and bioenergetic system impairment. By regulating energy synthesis and cell death, mitochondria play a crucial role in the functioning of cells. Increased formation of reactive oxygen species (ROS) and oxidative stress are a result of mitochondrial dysfunction, which also accelerates the development of Alzheimer's disease. For the maintenance of balance, autophagy is crucial because it selectively destroys damaged mitochondria. AD affects this route for mitochondrial breakdown. Targeting specific mitochondrial ligands by interventions along this pathway might be a useful therapeutic approach. Due to a number of biological obstacles, this method has significant limitations. As a result, many nanocarriers have been created to improve drug delivery effectiveness. All potential nanotechnology-based treatments for AD have been examined in this study, with a particular emphasis on medication delivery to the mitochondria

Keywords

Alzheimer’s disease; Quantum Dot Nanoparticles; PINK1; Theranostic; mitochondria; drug delivery

Subject

Medicine and Pharmacology, Neuroscience and Neurology

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