Abstract

*Satish Bhagwan Bramhane, Pritam Bhagwan Patil and Swapnali Pankaj Mahajan

ABSTRACT

Alzheimer's disease (AD), the most frequent cause of dementia, is escalating as aglobal epidemic, and so far, there is neither cure nor treatment to alter itsprogression. The most important feature of the disease is neuronal death and loss ofcognitive functions, caused probably from several pathological processes in thebrain. The main neuropathological features of AD are widely described as amyloidbeta (Aβ) plaques and neurofibrillary tangles of the aggregated protein tau, whichcontribute to the disease. Nevertheless, AD brains suffer from a variety ofalterations in function, such as energy metabolism, inflammation and synapticactivity. The latest decades have seen an explosion of genes and molecules that canbe employed as targets aiming to improve brain physiology, which can result inpreventive strategies for AD. Moreover, therapeutics using these targets can helpAD brains to sustain function during the development of AD pathology. Here, wereview broadly recent information for potential targets that can modify AD throughdiverse pharmacological and nonpharmacological approaches including genetherapy. We propose that AD could be tackled not only using combination therapiesincluding Aβ and tau, but also considering insulin and cholesterol metabolism,vascular function, synaptic plasticity, epigenetics, neurovascular junction andblood–brain barrier targets that have been studied recently. We also make a case forthe role of gut microbiota in AD. Our hope is to promote the continuing research ofdiverse targets affecting AD and promote diverse targeting as a near-future strategy.