Our brains change as we age. Many of us notice slower thinking and problems with recalling certain events as we grow older; nonetheless, confusion, memory loss and other key changes in how our minds work may be a sign that brain cells are failing. Many people confuse Alzheimer’s disease with dementia. Dementia is a set of symptoms that include problem solving, reasoning skills and memory loss while Alzheimer’s disease is a progressive disorder that is usually characterized by considerable dysfunctions in cognition, functionality, and behavior (Sabbagh et al., 2011). Researchers have discovered changes that take place in the brains of those who have Alzheimer’s disease that may cause the memory loss and decline in other mental abilities that occur with Alzheimer’s disease. While it is not entirely understood why these brain changes occur, scientists have been searching for underlying factors that may lead to Alzheimer’s disease. Such precursors include an increase in Amyloid β peptides, a decrease in the neurotransmitter acetylcholine, and the demyelization of the myelin sheath.
Throughout the process of aging the concentrations of acetylcholine decrease resulting in irregular lapses of short-term memory. Once acetylcholine is released into the synapse, a protein (acetylcholinesterase) breaks it down. Acetylcholinesterase is required to ensure that acetylcholine does not stay in the synapse for an excessive amount of time; if it remains in the synapse too long it can impair the brain's health. Acetylcholine is important for the functions of many different nerves and is particularly important for parts of the brain involved in memory and learning because they use acetylcholine extensively (Chu et al., 2005). Notably, acetylcholine levels are lower in people with Alzheimer's disease. This suggests that the loss of acetylcholine-secreting neurons may cause some of the symptoms of Alzheimer's disease.
Alzheimer’s disease is characterized by the presence of neurofibrillary tangles and neurotic plaques that are formed by β-amyloid deposits (Quirion, 1993). The accumulation of these β-amyloid peptides in Alzheimer's disease plays a contributing role in triggering synaptic dysfunction in neurons (Lefort et al., 2012). It was found that amyloid β1-42 peptides (Aβ1-42) play a key role in the pathogenesis of the cholinergic dysfunction in Alzheimer’s disease (Hoshi et al., 1997). Since cholinergic cells play an important role in memory and learning, any damage done to these cells will become dysfunctional. There is an increase in soluble Aβ1-42 that may agitate cholinergic functions, leading to the decline of memory and cognitive functions that are characteristics of Alzheimer’s disease. Hoshi et al (1997) hypothesized that soluble Aβ1-42 is produced at an early phase of Alzheimer’s disease and can start effecting cholinergic neurons by repressing acetylcholine synthesis, thus causing a drop in acetylcholine release, modulating synaptic connections, and finally resulting in cholinergic deficits, in which may provoke progressive loss of memory and cognitive function in patients with Alzheimer’s disease. Therefore, soluble Aβ1-42 may have a principal role in the cholinergic dysfunction in the formation of Alzheimer’s disease by suppressing acetylcholine synthesis.
White matter, or myelin, coats and insulates neuronal axons. Nonneuronal cells called oligodendrocytes wrap around the axon; these oligodendrocytes create the thickness of the myelin coats around the axon and control the speed of electrical impulses that affects processing of information (Fields, 2010). Loss of myelin is associated with Alzheimer’s disease (Sjobeck et al., 2005); this demyelization could be an explanation for Alzheimer’s disease. The white matter consists of millions of bundled axons that connect neurons in different parts of the brain. Myelin is vital for high-speed transmission and any damage done in such regions...
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