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Alzheimer’s disease
Alzheimer’s disease is a kind of degenerative disease that affects the neurological system, in particular, the brain. It normally has a slow onset and over time the symptoms get worse. It is the root cause of 60-70% of the dementia cases and its most prominent symptom is that the patients experience increasing difficulty in remembering some recent memories. As the disease progresses its symptoms get worse including the development of problems with language, lack of motivation, behavioral problems, mood swings, and disorientation. As the disease progresses the condition of the patient deteriorates and eventually they withdraw from family and society. Over time, the loss of brain functioning leads to loss of bodily functions which in the long run leads to death.
The rate of progression of the disease varies between individuals but normally the average life expectancy after diagnosis ranges between three to nine years. The primary cause of Alzheimer’s disease is not well understood but genetics is believed to play a very significant role in determining an individual’s chances of developing this neurodegenerative disease (Van Cauwenberghe et al., 2016). There are a number of other risk factors for the development of Alzheimer’s which include hypertension, depression and a history of head injuries. The disease process of Alzheimer’s is linked to the development of clearings referred to as plaques in the brain. The disease also leads to the development of neurofibrillary tangles in the brain.
The signs and symptoms of Alzheimer’s disease depend on the stage of the disease. There are three major stages of progression of the disease which are the early, middle and late stages of the disease. During the early stages of the disease, the most prominent symptoms include forgetting names of friends and family, changes in attitude and behavior which are only noticeable to close friends and family, confusion in situations that are not familiar, episodes of forgetfulness. In the middle stages of the disease, the most noticeable symptoms include increasing difficulty in remembering recently acquired information, sleeping problems, problems with determining their location, increasing levels of confusion in most circumstances. During the later stages of the disease the patients experience difficulty in thinking and reasoning, speaking problems, they tend to repeat their conversations and become more abusive and paranoid (Calsolaro and Edison, 2016). Before this three major stages begin there is a pre-dementia stage during which the symptoms are easily mistaken for those linked with stress and aging. Such early symptoms have the capacity to affect more complex activities that a person carries out every day. Loss of short term memory is the most noticeable deficit which is demonstrated by difficulty in remembering recently acquired facts or information. As the disease of signs of progress the patient loses most of their brain function leading to increased memory loss, loss of cognitive ability, and in the long run they are unable to depend on themselves which makes it necessary for them to be placed under medical care in a hospital or nursing home setting (Kerr et al., 2017). Towards the late stages of the disease, the patient loses their ability to carry out normal functions such as movements due to muscle spasm which in most cases makes them bedridden. In the long run, death results even though the cause of death is normally attributed to external factors such as pneumonia or even bedsores from lack of movement.
Diagnosis of Alzheimer’s disease is normally based on the medical history of the patient, observation of behavior and history of relatives with the disease. The presence of certain neuropsychological and neurological characteristics that are associated with Alzheimer’s and lack of alternative conditions are all used to confirm a diagnosis. There are a number of techniques that have in the recent past been adopted for the diagnosis of Alzheimer’s such as computed tomography (CT), positron emission tomography (PET), medical imaging among other are helpful in excluding other cerebral pathologies. The assessment of intellectual functioning such as testing of memory capabilities is also used to further identify the stage of the disease. In the recent past, medical organizations have come up with a diagnostic criterion that make it easy to confirm a diagnosis by standardizing the processes used for diagnosis performed by medical practitioners. Diagnosis of Alzheimer’s disease can be confirmed through the performance of post-mortems on the brain which are very accurate and can this can also be done through histological examination. Neuropsychological screening tests are very resourceful in the diagnosis of Alzheimer’s. During such tests, the patient is called on to copy drawings that look alike to the ones shown in the picture, read, memorize words and subtract numbers. Mini-mental state examination (MMSE) is an example of a neuropsychological test that is commonly used to determine the level of cognitive impairment of the disease which is required for diagnosis. A more comprehensive range of the test is required in order to obtain highly reliable results especially during the initial stages of the disease. Neurological examination is one of such early diagnosis techniques which are used to differentiate the cognitive impairment of Alzheimer’s from that of another disease such as dementia.
The processes of Alzheimer’s disease are that the disease causes loss of synapses and neurons in the cerebral cortex region of the brain. This degeneration of these essential components of the brain leads to gross atrophy of the regions of the brain that are affected which includes the cingulate gyrus, frontal cortex, parietal and temporal lobes. The degeneration also occurs in the locus coeruleus which is one of the brainstem nuclei (Palop and Mucke, 2016). The existence of neurofibrillary tangles as well as amyloid plaques can be confirmed through microscopy of brain slides specimens obtained from the histological specimens of patients. The plaques are formed from deposits of beta-amyloid peptide which are dense and insoluble in a combination of cellular materials on the exterior and outside of the neurons. Tangles are aggregations of proteins such as tau which are deposited inside the cells.
Based on research on twins and families the genetic heritability ranges from 49 to 70%. About 1% of these cases are linked with the familial forms of autosomal dominant inherited factors which normally cause the disease to have an early onset usually earlier than 65years (Wes et al., 2016). These are associated with early-onset familial Alzheimer’s disease. These genetic factors are associated with mutation of a couple of genes that encode for amyloid precursor protein (APP). The mutations in genes that encode for these genes lead to increased production of the APP protein as well as other kinds of proteins that are associated with the development of senile plaques. Most cases of Alzheimer’s disease are not as a result of autosomal dominance and are as a result referred to as sporadic Alzheimers disease whereby environmental factors and genetic variance are risk factors.
In regards to biological medications, there are a number of drugs such as donepezil, the 3-D molecular model used in the treatment of Alzheimer’s disease. Donepezil is a kind of medication that is used for the acetylcholinesterase inhibitor used in the treatment management of the symptoms of Alzheimer’s (Mendiola-Precoma et al., 2016). Memantine is a kind of medication with a molecular structure which has been approved for the treatment and management of the symptoms of advanced Alzheimer’s.
Currently there five kinds of medications used in the treatment of cognitive problems associated with Alzheimer’s disease. These include acetylcholinesterase inhibitors such as donepezil, galantamine, tacrine, and rivastigmine. However, such medications have a limited effect on reversing or slowing down the advancement of Alzheimer’s since no medication has been demonstrated to slow down or stop the progression of Alzheimer disease. The lowered activity of the cholinergic neurons is one of the most noticeable effects of Alzheimer’s disease. As such Acetylcholinesterase inhibitors are taken to reduce the rate of breakdown of acetylcholine which is as a result of the destruction of cholinergic neurons. Such drugs have a mild to moderate efficacy in the reduction of cognitive impairment associated with the advanced stages of the disease.
In general Alzheimer’s is one of the most common degenerative disorders of the brain. It usually has a slow onset and even slower progression. The advanced stages are characterized by loss of cognitive function such as loss of memory capability, loss of speech, reduced physical activity and paranoia. Eventually, the patient loses their independence and withdraws from family and friends. Death is usually the result of Alzheimer’s disease mostly due to external factors.
References
Calsolaro, V., & Edison, P. (2016). Neuroinflammation in Alzheimer’s disease: current evidence and future directions. Alzheimer’s & Dementia, 12(6), 719-732.
Kerr, J. S., Adriaanse, B. A., Greig, N. H., Mattson, M. P., Cader, M. Z., Bohr, V. A., & Fang, E. F. (2017). Mitophagy and Alzheimer’s disease: cellular and molecular mechanisms. Trends in neurosciences, 40(3), 151-166.
Mendiola-Precoma, J., Berumen, L. C., Padilla, K., & Garcia-Alcocer, G. (2016). Therapies for prevention and treatment of Alzheimer’s disease. BioMed research international, 2016.
Palop, J. J., & Mucke, L. (2016). Network abnormalities and interneuron dysfunction in Alzheimer disease. Nature Reviews Neuroscience, 17(12), 777.
Van Cauwenberghe, C., Van Broeckhoven, C., & Sleegers, K. (2016). The genetic landscape of Alzheimer disease: clinical implications and perspectives. Genetics in Medicine, 18(5), 421.
Wes, P. D., Sayed, F. A., Bard, F., & Gan, L. (2016). Targeting microglia for the treatment of Alzheimer’s Disease. Glia, 64(10), 1710-1732.
