**5. Alzheimer's disease (AD)**

The Alzheimer Association attributes 60–80% of dementia cases to Alzheimer's disease (AD), a degenerative brain illness. Depending on the stage of the illness, apathy, depression, decreased communication, disorientation, poor judgment, difficulties swallowing and walking, and behavioral changes are some of the characteristics that evolve to make doing daily tasks difficult [32, 33]. Age, genetics, and sex are some of the factors that influence how long it takes for a continuum of these symptoms to emerge, according to current estimates, and the COVID-19 pandemic has seen a 16% increase in the number of deaths (Alzheimer's Association, 2021). Amyloid-beta (Aβ) and tau protein buildup is linked to the progression of cognitive deterioration in AD. Beta-secretase and gamma-secretase sequentially cleave the amyloid precursor protein (APP), resulting in the formation of Aβ. Thus, the aggregation of Aβ produces hazardous oligomers for the neurons. Tau, on the other hand, is produced by alternative splicing from the soluble protein isoforms of the microtubule-associated protein tau (MAPT) gene. The damage to brain circuits and cognitive impairment in AD has been linked to a number of functional interactions between Aβ and tau. In the neuropathology of Alzheimer's disease, there is a loss of neurons and atrophy in the temporofrontal cortex, which results in inflammation and the deposition of amyloid plaques, an abnormal cluster of protein fragments, and tangled bundles of fibers. As a result, there is an increase in the presence of monocytes and macrophages in the cerebral cortex, and it also activates the microglial cells in the parenchyma [34–36].
