Alzheimers Disease

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 ? 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 ? -amyloid deposits (Quirion, 1993). The accumulation of these ? -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 ? 1-42 peptides (A? 1-42) 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 A? 1-42 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 A?

1-42 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 A? 1-42 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 can impair sensor, motor, and cognitive functions (Fields, 2010). When demylination occurs, the nerve fibres affected would have inhibited action potentials, which would slow down the signal. Eventually, with increased demylination, that signal could potentially cease to transmit signals altogether and may effect the retrieval of memories and facts of one’s own life. Sjobeck et al (2005) noted that the anterior part of the brain is more heavily affected by myelin reduction than the posterior.

The anterior section of the brain contains the frontal cortex, which is involved in thinking, judgement, and higher level functioning. Myelin loss in this section of the brain could severely impact those functions and be a significant factor in Alzheimer’s disease. Acetylcholine has two receptors: the nicotinic receptor and the muscarinic receptor. The nicotinic cholinergic systems are involved in cognitive functioning including learning and memory (Chu et al. , 2005). Since acetylcholine has such a strong effect on memory and learning, it is notable that acetylcholine impacts these nicotinic receptors.

A subtype of a nicotinic receptors, ? 7, is found largely in astrocytes (found in the central nervous system), and creates inflammation that aids in the deterioration process of neurons. Using immunochemistry it was found that astrocytic intracellular calcium induces neuronal cell death, particularly in the hippocampus (Taektong et al. , 2004). The hippocampus plays vital roles in long-term memory. Any damage done there would impair the hippocampuses functions; therefore, degeneration in this area would cause Alzheimer’s disease-like symptoms.

While the nicotinic receptor plays a role in the formation of Alzheimer’s disease, the muscarinic receptor plays a role in the treatment of the same disease. Degeneration of neurons is the main cause of Alzheimer’s disease, but a high level of cholesterol is a large factor as well. Treating degeneration can be extremely difficult. However, focusing on decreasing the levels of cholesterol can show the same positive effects as treating degeneration for those on the threshold of Alzheimer’s disease.

Treating cholesterol with M1 muscarinic acetylcholine receptor (M1-MAChR) agonists may provide a practical way to reduce squalene synthetase activity level (high squalene synthetase activity is a key precursor in cholesterol), thus decreasing the chance of receiving Alzheimer’s disease, and helping those who live with the disease (Zuchner et al. , 2005). In addition, Kojro et al (2010) hypothesized that cholesterol lowering drugs such as statins could have a healing potential in the prevention and treatment of Alzheimer’s disease.

These studies wanted to find the precursors of Alzheimer’s disease. Scientists and researchers are searching for not only medicine to combat this disease, but also a way to cure it. While going over the studies, the main signs of Alzheimer’s disease are having prominent neuron death in the hippocampus, and the gradual death of cholinergic brain cells. The topic of how these brain deficits effect Alzheimer’s disease is important because the more we learn about how and why this disease can occur the better chance we have to control and perhaps even terminate the disease completely.

References Chu, L. & Ma, E. & Lam, K. & Chan, F. & Lee, D. (2004). Increased Alpha 7 Nicotinic Acetylcholine Receptor Protein Levels in Alzheimer’s Disease Patients. Dement Geriatr Cogn Disord. Retrieved from: DOI 10. 1159/000082661 Fields, R. (2010) Change in the Brain’s White Matter. Science, 330. Retrieved from: doi 10. 1126/science. 1199139 Hoshi, M. & Takashimi, A. & Murayama, M. & Yasutake, K. & Yoshida, N. & Ishiguro, I. & Hoshino, T. & Imahori, K. (1997). Nontoxic Amyloid ?

Peptide1-42 Suppresses Acetylcholine Synthesis: POSSIBLE ROLE IN CHOLINERGIC DYSFUNCTION IN ALZHEIMER’S DISEASE. The Journal of Biological Chemistry, 272. Retrieved from: doi 10. 1074/jbc. 272. 4. 2038 Kojro, E. & Fuger, P. & Prinzen, C. & Kanarek, A. & Rat, D. & Endres, K. & Fahrenholz, F. & Postina, R. (2010) Statins and the Squalene Synthase Inhibitor Zaragozic Acid Stimulate the Non-Amyloidogenic Pathway of Amyloid-? Protein Precursor Processing by Suppression of Cholesterol Synthesis. Journal of Alzheimer’s disease. Retrieved from: 10. 3233/JAD-2010-091621.

Lefort, R. & Pozueta, J. & Shelanski, M. (2012). Cross-linking of cell surface amyloid precursor protein leads to increased ? -amyloid peptide production in hippocampal neurons. Implications for Alzheimer’s disease. US: Society for Neuroscience, Vol 32(31). Retrieved from: doi 10. 1523/JNEUROSCI. 6473-11. 2012 Quirion, R. (1993). Cholinergic markers in Alzheimer disease and the autoregulation of acetylcholine release. Journal of Psychiatry and Neuroscience, vol 18(5).

Retrieved from: http://www. ncbi. nlm. nih. gov/pmc/articles/PMC1188543/? page=1 Sabbagh, M.& Cummings, J. (2011). Progressive cholinergic decline in Alzheimer’s Disease: consideration for treatment withdonepezil 23 mg in patients with moderate to severe symptomatology. BMCNeurology, 11:21. Retrieved from: doi 10. 1186/1471-2377-11-21 Sjobeck, M, & Haglund, M. & Englund, E. (2005). Decreasing myelin density reflected increasing white matter pathology in Alzheimer’s disease—a neuropathological study. Wiley InterScience. Retrieved from: doi 10. 1002/gps. 1384 Taektong, T. & Graham, A. & Court, J. & Perry, H. & Jaros, E. & Johnson, M. & Hall, R. & Perry, E.

(2004). Nicotinic acetylcholine receptor immunohistochemistry in Alzheimer’s disease and dementia with Lewy bodies: differential neuronal and astroglial pathology. Elsevier, Vol 225. Retrieved from: http://dx. doi. org. ezproxy. kwantlen. ca:2080/10. 1016/j. jns. 2004. 06. 015 Zuchner, T. & Schliebs, R. & Perez-Polo, J. R. (2005). Down-regulation of muscarinic acetylcholine receptor M2 adversely affects the expression of Alzheimer’s disease-relevant genes and proteins. Journal of Neurochemistry, Vol 95. Retrieved from: doi 10. 1111/j. 1471-4159. 2005. 03335. x.

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