Axonal Death And Alzheimer 's Disease

“Who are you?” “Do I know you?” Alzheimer’s disease is a very traumatic and disheartening disease that can affect loved ones in our families and relationships. I will be discussing the causes and prevention of this disease even though scientific facts and research are still being tested for validity.

Alzheimer’s disease causes atrophy to parts of the brain, specifically in brain tissue, as a loss of neurons occurs in most patients.

- Lost keys, an overlooked name, requiring an additional minute to recall where you stopped your auto. No doubt we 're talking average absentmindedness or simply ordinary age-related changes, not Alzheimer 's ailment. In any case, when you start battling with errands that have dependably been simple (e.g., abruptly not having the capacity to adjust the checkbook) that is more reason for concernsaid by Nancy Udelson. Despite the way that 5.1 million individuals age 65 and more seasoned are as of now influenced by Alzheimer 's, it is not a "typical" some portion of maturing (however the danger rises with age). It is a dynamic issue that assaults the cerebrum 's nerve cells, clarifies Ditty Steinberg, the official VP of the Alzheimer 's Establishment of America. The brains of individuals who have Alzheimer 's are stopped up with injuries that conform to the outside of neurons, eventually annihilating these mind cells. As the person born after WW2 populace gets more established, the rate of Alzheimer 's is anticipated to blast, influencing upwards of 16 million individuals by 2050, unless therapeutic achievements distinguish approaches to forestall or all the more viably treat the illness. In the event that you have relatives who have experienced Alzheimer 's, you may think about whether you 're at higher danger, however just the "early onset" type of the malady (which influences individuals more youthful than 65 and records for under 5 percent of all cases)

Some area’s affected by neuronal loss are the cerebral cortex, the hippocampus, locus coeruleus, and cerebellum. Even with a single TBI, neuronal loss does occur, and evidence suggests this neuronal loss continues beyond the initial injury phase. White matter degeneration does occur as well, and while this study has little information on this, it is noted that white matter injury as well as axonal pathology has been suggested as a mechanism of rapid Aβ genesis. Also seen in neurodegeneration is neuroinflammation that is beyond repair. This inflammation continues after the initial injury in the white matter region, including the corpus callosum. Finally, changes in the cerebellar pathology are noted, in particular loss of cerebellar neurons. Smith, Johnson, & Stewart (2013) note atrophy and demyelination of the folial white matter present in those affected by

Alzheimer’s dementia is responsible for 60-80% of dementia cases and is the 6th leading cause of death in America (Alzheimer’s Association). Once diagnosed there’s no escaping it’s grip. The severity and rapid progressive state of the disease make Alzheimer’s a rather excruciating disease. Alzheimer’s affects groups of nerves in the brain. Doctors believe it prevents the nerve “factories” from running correctly and prolonged back up in a single grouping of nerves begins to affect those surrounding/connected to it (Alzheimer’s Association). As the damage spreads, cells begin to die and cause serious irreversible brain damage. Nerve damage occurs before there is any signs that the patient is developing dementia, and by the time early signs of Alzheimer’s dementia begin to appear there is already significant amount of the brain that has been touched and can no longer to salvaged.

Why might this be? At the cellular level, why does the wearing down of neurons give Cecil difficulty walking in the beginning of the story? It was not directly stated in the case study, but why is ALS fatal?

Although, causes are still unknown about how the disease started, researchers are aware that the damage in the brain begins 10 to 20 years before changes are noticeable. Two main features in the brain which were introduced earlier in this paper are the amyloid plaques, they are found in gaps between nerve cells of the

The common pathological feature of HSP includes distal axonal degeneration, which is most severe in the terminal ends of fibers within the cortico-spinal tract (figure 1.1) (Blackstone, 2012 and Noreau et al., 2014). The cortico-spinal tract is the main pathway involved in voluntary movement in which neurons originating within the cerebral motor cortex travel relatively long distances to make synaptic connections with lower motor neurons terminating in skeletal muscle (Blackstone et al., 2010). Axons within the cortico-spinal tract are therefore some of the longest motor neurons within the body,

Alzheimer’s disease is a neurodegenerative disease that disrupts a person’s memory, thinking abilities, and behavior. This disease affects three major areas in the brain; the cerebrum, the cerebellum, and the brain stem. As the disease begins to take effect, these parts of the brain become obstructed, and the information that is supposed to be transmitted between neurons is hindered. The information that is responsible for sensory, learning, and memory progressively digress’ in productivity. Alzheimer’s disease causes nerve cell death and tissue loss all around the brain, which reduces the brain’s ability to function at a rapid pace and comprehend basic signals (“Alzheimer’s & Dementia,”n.d.). As parts of the brain begin to deteriorate, normal functions begin to drift away as well.

ALS is inherited in five to ten percent of cases, while other cases just seem to appear randomly (Learn About ALS 2014). Some believe that the nerve cells that control movement just gradually die off. It is also said by doctors and scientists that this condition is the result of a gene mutation. Others, on the other hand, believe there is a chemical imbalance where there are higher than normal levels of glutamate, which is a chemical messenger in the brain around the nerve cells in their spinal fluid (Learn About ALS 2012). Earlier in class, we established that glutamate is a salt or ester of glutamic acid, and too much glutamate is known to be toxic to some nerve cells. Some cases could be a result of a disorganized immune response where the immune system begins attacking normal cells, leading to the death of nerve cells. When a body’s own cells begin attacking its normal cells, it’s almost guaranteed that the body is at risk for shutting down. There could also be some sort of protein mishandling; mishandled proteins with the nerve cells may lead to gradual accumulation of abnormal forms of these proteins in the cells, eventually causing nerve cell death. Some scientists believe that they have found genetic links related to acquiring this disease, but not legitimate cure has been settled on or established (Learn About ALS

The evidence of neurofibrillary tangles is important to diagnosis. Inside the neurons, there will be abnormal clumps of tau protein. Tau protein normally attaches to microtubules of the neuron and acts as its stabilizer. Abnormal chemical changes cause Tau proteins to detach from the microtubules and stick to other tau proteins, forming threads, which clump together—tangles. Tangles may block the synaptic signaling between the neurons. Neurons will eventually begin to die and as this spreads, regions begin to shrink. The final stage will have widespread damage and significant shrinkage. Scientists are looking for specific types of cell death, which are found in normal aging, but greater in AD and the location matters. The brain will also show signs of inflammation in response to cellular injury (22, 23).

Alzheimer’s disease is six out of the ten leading causes of death in the U.S. and five out of the ten leading causes of death in elderly people over the age of 65. AD diagnosis occurs through postmortem detection of pathology in neural tissue. The risk of getting AD comes within age. Individuals with MCI are at risk of progression to getting AD. Close to 15 percent of adults above the age 65 are diagnosed with MCI, and more than half of them develop AD more quickly. MCI adults can regain cognitive function by exercising, eating healthy, reducing cholesterol intake, and by working the memory by practicing challenging cognitive tasks. Working memory is a system that underpins cognitive activities ranging from attention to a specific stimulus

Taking a closer look at the cerebrum, allows us to have a better understanding of the dying-forward cascade and its important role in initiating disease onset (Thomsen, et al., 2014). The outer layer of this complex organ composed of gray matter is the cerebral cortex, region where the corticospinal neurons related to ALS are located. These upper motor neurons responsible for collecting, integrating, translating, and transferring information to the spinal cord reside in layer 5 of the motor cortex (Thomsen, et al., 2014), and are the most vulnerable to be injured by excitotoxicity initiating an anterograde degeneration. In general, ALS research has devoted less attention to the UMN pathology primarily focusing on the LMN connectivity with the neuromuscular junction (NMJ) (Thomsen, et al., 2014). In spite of this remark, recent studies continue to use spinal cord neurons from transgenic SOD1 mice but their priority has switched to the UMN behavior. On a study using mutant SOD1G39A rats, (Thomsen, et al., 2014) wanted to establish whether the upper motor neuron might still play a critical role in disease progression by knocking down mutant SOD1expression in only the motor cortex. As a consequence of this assay, it was shown for the first time that suppression at the top of the motor neuron pathway results in significant delay in ALS disease onset. Thus, further highlighting the importance of the upper motor neurons in ALS (Thomsen, et al., 2014).

Accordingly, a recent study showed that injections of MSC-CM in a SCA-1-Knock-in mice model improved motor coordination as the factors released by MSCs, namely the hepatocyte growth factor (HGF), were able to ameliorated the degeneration of axon and myelin of spinal motor neurons (Suto et al. 2016). Such improvements were similar to those obtain in a previous work where mice of the same model were treated only by MSCs administration (Mieda et al.,

A distinctive characteristic of ALS is that although the motor neurons die, the brain, cognitive functions and sensory neurons stay intact (Porth & Matfin, 2009). This makes the disease especially devastating because patients become trapped inside their dying body, with a fully alert mind, but are unable to move. It is not known what causes the exact death of the motor neurons in the body, but “five percent to 10% of cases are familial; the others are believed to be sporadic” (Porth & Matfin, 2009, p.