Alzheimer’s Disease: Pathogenesis and Therapeutic Interventions

Abstract

Background: Alzheimer’s disease (AD) is the most common cause of dementia. Genetics, excessive exposure to environmental pollutants as well as unhealthy life style practices are often linked to development of AD. No therapeutic approach has achieved complete success at treating AD; however, early detection and management with appropriate drugs is key to improving prognosis. Interventions: The pathogenesis of AD was extensively discussed in order to understand the reasons for the interventions suggested. The interventions reviewed include the use of different therapeutic agents and approaches, gene therapy, adherence to healthy dietary plans (Mediterranean diet, Okinawan diet and MIND diet), as well as the use of medicinal plants. The potentials of nanotechnology as a multidisciplinary and interdisciplinary approach in the design of nanoformulations of AD drugs and the use of superparamagnetic iron oxide nanoparticles (SPIONs) as theranostic tools for early detection of Alzheimer’s disease were also discussed.

MRI measurements of brain hippocampus volume in relation to mild cognitive impairment and Alzheimer disease: A systematic review and meta-analysis

“…It is an acquired progressive cognitive disorder that affects activities of daily living and is a major cause of dependence, disability and death. [4,25,26] Current estimates suggest that 44 million people worldwide are currently living with dementia. This number is expected to more than triple by 2050 as the population ages, when the annual cost of dementia in the United States alone could exceed $600 billion.…”

DNA methylation: The epigenetic mechanism of Alzheimer's disease

“…The role of inflammatory mechanisms triggered by cytokines in the pathogenesis of AD has been somewhat elucidated. 58 Tumor necrosis factor-α (TNF-α) plays a crucial role in promoting inflammation and pro-apoptosis. TNF-α induces neuronal apoptosis through TNF-α p55 receptors constitutively expressed in a pan-neuronal pattern and inflammation through TNF-α p75 receptors.…”

“…The role of inflammatory mechanisms triggered by cytokines in the pathogenesis of AD has been somewhat elucidated. 58 …”

Chicoric Acid Ameliorated Beta-Amyloid Pathology and Enhanced Expression of Synaptic-Function-Related Markers via L1CAM in Alzheimer’s Disease Models

“…According to the World Health Organization (WHO), by 2030, the number of people with AD will increase to 82 million, and dementia will become a global crisis [ 2 ]. The pathological features of AD include the accumulation of Aβ plaques and the hyperphosphorylation of tau protein [ 3 ]. Amyloid-β is formed by the cleavage of amyloid precursor proteins (APPs) via β-secretase (BACE1) and γ-secretase.…”