Alzheimer’s Disease Report
Alzheimer’s disease is the top 10 fatal diseases that doesn’t have a cure, no means of prevention, and no disease-modifying treatment. Alzheimer’s disease isn’t just a disease that affects older aged people, there have been hundred, maybe even thousands of patients who have shown symptoms of Alzheimer’s during their 40’s, 50’s, or even in their 30’s. Although it is just about 5% of the time, whenever this happens to someone it’s referred as Alzheimer’s early on-set. In addition, about 700,000 people die from Alzheimer’s and dementia; this makes it the third leading cause of death behind cancer and heart disease. Unfortunately, the only thing we have against Alzheimer’s are treatments that help slow down the symptoms
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Nevertheless, Alzheimer’s can be a mutation in the genes and trigger Alzheimer’s to arise, however which genes are involved that trigger this disease? In addition, Alzheimer’s attacks the brain, but which brain regions does it attack, and what is the molecular structure of Alzheimer’s disease? The gene involved during Alzheimer’s early onset is in a mutation that occurs in Chromosome 14. However, various chromosomes play a key role when developing Alzheimer’s. Amyloid precursor protein (Chromosome 21) was discovered in 1987 to be the first gene that causes mutations that cause an inherited form of Alzheimer’s. In addition, Presenilin-1(Chromosome 14) was later discovered in 1992, that this Chromosome has the most common mutations to inherit Alzheimer’s. In 1993, Presenilin-2(Chromosome 1) was discovered that it as well had mutations that …show more content…
We all know it’s in the brain, however, which part of the brain does it attack? At first, it attacks neurons that have connections that are involved in memory. Later on, it moves towards the basal forebrain and the hippocampus, and then later on areas in the cerebral cortex that are involved in language, reasoning and social behavior. Nevertheless, the brain shall start getting smaller as the disease progresses even further. Some of the most affected or damaged areas after Alzheimer’s is the hippocampus, which is used for storing new memories as well as the cortex that is used for thinking, planning and remembering. However, the lateral ventricles grow larger. In addition, for example, in a healthy brain gene TREM2 that is in charge of microglial cells telling them to help clean up debris, waste, and kill pathogens in the brain to protect the neurons especially from beta-amyloid, which is a dangerous toxin in the brain. However, in a brain that has Alzheimer’s Chronic inflammation is possible due to the buildup of microglial cells. Nevertheless in Alzheimer’s there are neurofibrillary tangles inside neurons, the tangles involve a protein called tau, which bind together microtubules in the brain of a patient suffering from Alzheimer’s it then grabs onto other tau molecules which then form a spaghetti-like tangles which end up killing neurons due to these tangles
The symptoms of Alzheimer’s are extremely detrimental to the individual whom it affects, as the disease attacks the brain cells and their connections. As the illness progresses, many
Alzheimer’s disease affects the entire brain eventually, but as it moves through the different stages it may affect certain areas more. Before any side effects of the disease become observable, decades of damage to the brain can take place. This is known as the preclinical stage of Alzheimer’s disease. This damage is believed to take place primarily in the hippocampus, where memory functions in the brain. Here is where plaques and neurofibrillary tangles form and cause neuron death, which spreads the damage to other areas of the brain.
Due to the inability of the brain to replace nerve cells, some brain function is lost. The key question in Alzheimer’s disease is, what causes the neuron degeneration (Johnson, 1989)? The focus for finding the cause is on abnormal structures found in the brain of people with Alzheimer’s. Unfortunately, the abnormal structures the brain undergoes still has researchers uncertain as to how they are involved in Alzheimer’s and exactly how the disease occurs.
Alzheimer's disease was described for the first time by Alois Alzheimer in Nov. 1901 when he met his 51-year-old patient Auguste D who had a progressive memory loss, cognitive decline and movement retardation. After the death of Auguste, Alzheimer had sent her brain to Munich for a thorough study to find out later that there are two lesions in the brain: senile plaque and neuro fibrillary tangle1. Senile plaques are extracellular deposits of amyloid-β and the majority species of it is Aβ40 and Aβ42, whereas the neuro fibrillary tangles are composed of defective tau filaments that are joined together inside neurons to form a round shaped tangle2.
Until recently, two significant abnormalities were observed in the brain of patients affected by Alzheimer's Disease: twisted nerve cell fibers, known as tangles neurofibrilares, and a protein called beta amyloid (Qué es la enfermedad de Alzheimer?, n.d., para. 3).
According to Lu and Bludau (2011), Alzheimer disease is a degenerative disease of the brain that can lead to dementia and impair all brain functioning. Biologically, Alzheimer’s disease is believed to be caused by abnormal plaques called amyloid plaques, which are a buildup of protein fragments that are thought to be damaging to the brain cells. However, scientists are still unsure if this buildup actually cause the disease or is a result of the disease itself. This disease can also be a result of a genetic mutation, increasing individuals with the gene mutation risk as much as eight times higher than individuals
Alzheimer disease (AD) is the most common cause of dementia in the elderly, accounting for 65–70% of all cases (Jellinger, Janetzky, Attems, & Kienzl, 2008). The other dementias are of the Parkinson 's group, the fronto-temporal group and the vascular group. The total worldwide yearly costs for the treatment and care of patients suffering from dementia are estimated to be around 250 billion US dollars. The lifetime risk for AD between the ages of 65 and 100 is 33% for men and 45% for women with an annual increase of 1–2% in the seventh decade to almost 60% in the 10th decade with doubling every 5 years (Jellinger et al., 2008). AD is incurable, and thus represents a major public health problem. AD represents a challenge to humanity due to its relatively recent discovery, progressive nature of the illness, and complex diagnosis.
Early-onset Alzheimer’s is a rare, but fast stage of Alzheimer’s disease. According to Glenn E. Smith, Ph.D., a neuropsychologist at Mayo Clinic, in Rochester, Minn. (2014), Early-onset Alzheimer’s is an uncommon form of dementia that strikes about 5 percent of patients with symptoms before the age of 65. This form of Alzheimer’s has been known to develop between the ages 30 and 40, but that’s very uncommon (Smith 2014). Scientists do not have an explanation of why people get the disease younger than others. Early-onset Alzheimer’s that is hereditary in family members is connected to three different genes that differ from the APOE gene that can increase your risk of Alzheimer’s in general (Smith 2014). The innate conduit of inheritance is much stronger in early-onset Alzheimer’s (Smith 2014). If one has a genetic mutation
One in three seniors die of Alzheimer’s disease or another form of dementia (Godman). Alzheimer’s disease is the most common form of dementia but all types of dementia diseases effect seniors and their families in a dramatic drastic way. Early signs of Alzheimer’s start as early as the age of 30 and can affect someone for the rest of their life. These diseases have become more reoccurring every year, effecting around 5.3 million Americans and will continue to change lives for the rest of time (Bender, 2). As of now, there has been no cure for Alzheimer’s but scientists and doctors are putting time and effort into an Alzheimer’s cure through research, trials and ways to prevent the disease.
Currently, more than five million Americans are living with Alzheimer’s Disease. Alzheimer’s has also worked its way up to the sixth leading cause of death in the United States. Not only does this disease take the lives of the victims, but it also takes a perhaps bigger toll on the caregivers. The longer a victim lives with Alzheimer’s, the more extensive time, effort, money, and caution a caregiver has to provide. Today, there is no cure for Alzheimer’s. However, there are new treatments that slow the progression of the disease, and there are also new ways for doctors to diagnose it earlier. It is amazing that something that affects so many people is so difficult to have
Alzheimer’s disease is a common problem in today’s society and within the older population this disease makes up the largest form of dementia. Although it is a problem in mainly older people, this disease can still occur in the younger population also. People in their 30s-50s can be diagnosed with this disease, even though it is not as common as people in their 60s-90s. The number of people with Alzheimer’s in the U.S. is close to five million and is expected to double within the next 30 years. With our modern medicine and advancements one would think a cure would be available, however, getting to the cause of the disease is a major factor. The cause of Alzheimer’s disease is one that is very debatable and questionable and most likely is a result of multiple factors rather than one. The main issue with finding the cause is because this disease affects the brain and can
With the growing number of people becoming diagnosed, and experiencing symptoms of Alzheimer’s disease, we must begin to take precautions and somehow attempt to gain knowledge of how the disease can be better treated, and ultimately prevented.
The research into Alzheimer's Disease has come a long way since 1906 when it is was discovered by Alois Alzheimer. He detected microscopic brain tissue changes called senile and neuritic plaques in deceased patients. These are chemical deposits consisting of protein molecules called Amyloid Precursor Protein(APP) that are fundamental components of a normal brain. However in the brain of an Alzheimer patient, an enzyme cuts the APP apart and leaves fragments in the brain tissue. These combined with degenerating nerve cells cause the plaques or lesions. These lesions are found in many sections of the brain including the hippocampus which regulates emotion and memory, the basal forebrain, and especially the basal nucleus of Meynert and the cortex, where the memory function is located.(2) Another sign of a diseased brain are neurofibrillary tangles, which are malformations within nerve cells.
According to most research, scientists, doctors and psychologists say that the causes of the brain damages are genetic factors, nutritional disorders, toxic exposure and radiation factors. In genetic factors, it is studied that Alzheimer’s disease can be caused due to hereditary. This is most commonly seen on patients who suffer the disease before the age of 50. In nutritional factors, scientists project some vitamin deficiencies can lead to Alzheimer disease.
The causes of Alzheimer’s are not yet fully understood; however, its effect on the brain can be understood. Alzheimer’s disease - insidious, attacking and terrifying - stalks and then murders brain cells. A brain afflicted with Alzheimer’s disease has a decreased count in cells and connections among cells. The more brain cells die, the smaller the brain of a person with Alzheimer’s gets. When doctors examine a brain with Alzheimer’s tissue, they see two types of deformities that are known to be trademarks of the disease. The first trademark is known as plaque, which is a cluster of a beta-amyloid protein that may damage and kill brain cells in a number of ways, including blocking with cell-to-cell communication. Whereas the final cause of brain-cell death in Alzheimer’s remains a mystery, the groups of beta-amyloids that cover the brain cells are a sure sign of the disease. The second trademark of Alzheimer’s is the tangle. Brain cells are reliant on internal support and a transport system to bring nutrients and other essentials to their distant regions. This system needs a protein called tau. In Alzheimer’s, strings of tau protein roll into abnormal tangles inside brain cells, concluding in failure of the cell's transport system. This breakdown of the system is powerfully involved in the decline and death of brain