Biochemical Changes Evidenced in Alzheimer's Disease: A Mini-Review
Luciana Scotti, Francisco Jaime Bezerra Mendonça Junior, Marcelo Sobral da Silva, Ivan R. Pitta and Marcus Tullius Scotti
Affiliation: Federal University of Paraíba Biotecnology Center 58051-970 João Pessoa PB Brazil.
Alzheimer’s disease is a brain disease that slowly destroys memory and thinking skills, and eventually, the ability
to carry out the simplest tasks. It begins slowly and gets worse over time. The main risk factor for Alzheimer's disease
is increased age. As a population ages, the frequency of Alzheimer's disease continues to increase. Currently, there is no
cure. There are many compromises in the brain of an Alzheimer's patient. Essentially, three modifications occur: decrease
of cholinergic impulse, increased toxic effects caused by ROS, and an inflammatory process in which amyloid plaque participates.
This study is a mini-review of Alzheimer’s disease, and we report advances in the studies concerning enzymes,
and substances or targets of these three processes. Our review was focused on a few biological pathways and involved in
the pathophysiology of AD: cholinergic system; oxidative stress; beta-amyloid processing; insulin signaling. We analyzed
a large body of evidence coming from biochemical studies and a series of compounds which act on these pathways as alternative
treatments for the disease.
Keywords: Acetylcholinesterase, Alzheimer’s disease, Amyloid plaques, Cholinergic impulse, Dementia, ROS.
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