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Introduction
Two neurodegenerative diseases such as Alzheimers disease (AD) and autism are not on the list of the most common conditions but have a significant effect on the patients well-being. Alzheimers disease is understood to be one of the most common central nervous system and mental pathologies, which usually affects people of advanced but active age. The opposite phenomenon is observed in autism spectrum disorder (ASD), which manifests itself in children from infancy or later in childhood. The choice of these conditions is not coincidental: modern physicians are increasingly convinced that there are definite similarities between dementia and autism spectrum disorders. This work is aimed at identifying differences and similarities in the mechanism of the formation of the described diseases and consideration of their progression.
Alzheimers Disease
One of the most common neurodegenerative diseases, Alzheimers disease, has a more than century-long history of study, and during this time, it has been investigated in sufficient detail. Alzheimers disease is considered to be a scourge of developed countries because, with increasing longevity, the probability of developing this type of senile dementia increases many times. The increased interest in the study of the disease may be dictated by statistical data, according to which the number of patients increases annually. According to a forecast given in the work of Alzheimers Association (2018), by 2050, the number of Americans who have Alzheimers will be about 14 million people, and today the disease has already caused the death of more than one hundred and ten thousand patients. Clinically, Alzheimers disease is usually characterized by progressive memory loss, followed by slow-progressing dementia.
The other neurodegenerative disease is associated with the inability to sufficiently initiate and maintain social interaction and social ties, as well as limited interests and frequently repetitive behavioral actions. In general, various forms of ASD are confirmed by 1% of the worlds population, with a more significant impact on boys (Kas et al., 2014). For this research paper, it is critical to note that autism spectrum disorders are a whole group of diseases that are combined with a wide range of abnormal behaviors.
ASD
For the wide variety of ASDs, there is a wide range of possible factors contributing to the development of genetic anomalies. Environmental causes are expected to have as strong an impact on autism risk as hereditary predisposition (Kas et al., 2014). In recent decades, researchers have explored the role of factors such as viral infections, vaccines, complications during pregnancy, or environmental pollution in the development of autism (Constantino & Charman, 2016). It is believed that the environment and lifestyles of parents before the birth of a child with ASD may include the use of drugs, alcohol, and environmental pollution (Ecker, Bookheimer, & Murphy, 2015). Air, water, and soil pollution with heavy metals and toxins complicate the situation: autistic children are tested for high levels of mercury, lead, aluminum, and other toxic metals.
Genetic mutation plays a crucial role in the development of ASD-related syndromes. Scientific studies have shown that autism is inherited, which means that autistic children who suffer from such a disease were initially genetically exposed to it at the embryo stage (Lord, Cook, Leventhal, & Amaral, 2000). Researchers have calculated that 65 genes are believed to be strongly associated with autism, and 100 genes that are weaker related to this diagnosis (Ecker et al., 2015). Moreover, disturbed expression of the genes may cause epigenetic modifications, such as DNA methylation. In support of genetics as a cause, studies showing that ASD is more common in boys than in girls can be added, most likely due to genetic differences associated with the Y chromosome (Lord et al., 2000). In autism, changes occur in areas of that part of the genome responsible for brain function and, in particular, the growth and conservation of synapses through which nerve cells can communicate with each other and with other cells.
It is assumed that the higher the socio-economic status of the family, the more accessible medicine is, and thus the probability of early detection of autism. According to Healy et al. (2008), it was found that, regardless of the socio-economic status indicators assessed by the study, children living in areas with lower socio-economic development are less likely to be diagnosed with ASD than their peers living in areas with higher socio-economic status (Healy et al., 2008). The study did not show better child health outcomes for ASD in the lower strata but rather lacked the necessary diagnosis, making it challenging to identify socio-economic factors.
Diseases Comparison
Alzheimers disease is associated with a small protein, ²-amyloid, whose insoluble deposits in nervous tissue have a devastating effect on higher nervous activity (Alexiou, Soursou, Yarla, & Ashraf, 2018). For this reason, the pathological and anatomical disease is characterized by a pronounced diffuse cortical atrophy. The main effect of the drug, according to the researchers, should have a direct impact on peptide sediments: in particular, destroy the protein aggregates or hinder their assembly (Alexiou et al., 2018). Together, this formed the basis for the most popular beta-amyloid hypothesis of the disease.
It is important to note that the causes of Alzheimers disease are still unknown. However, the main risk factors for Alzheimers disease are old age and a burdened family history. For example, there is extensive research showing that Alzheimers disease is hereditary (Alzheimers Association, 2018). The mutation in the PSEN1 gene is most likely associated with familial Alzheimers disease. The autosomal dominant type inherits it, in essence, one mutant copy of the gene is enough to affect: the first symptoms of the disease in the form of mild cognitive impairment occur at an average age of 44, and by the age of 50 dementia develops in such patients.
Another hypothesis concerning Alzheimers disease is the association with the neurotransmitter acetylcholine. AD is caused by increased damage to brain cells and consequent damage to the chemicals produced by them, known as neurotransmitters (Lanctôt et al., 2017). Among these neurotransmitters is acetylcholine, whose reduction plays a part in issues observed in people with Alzheimers disease. In answer to the beta-amyloid assumption, it is believed that the course of BA is more closely related to the loss of the soluble beta-amyloid form, which may disturb the generation and release of acetylcholine and prevent the activity of the substance involved in the maintenance of the structure and function of cholinergic neurons.
A large number of people on the planet are convinced that the source of various diseases is the psychological state of the patient similar views can often be heard about AD. There is no confirmed scientific evidence on the subject, but psychosomatic people tend to claim that Alzheimers is a peculiar way of escape from reality. Psychologists compare the course of the disease to the mental and emotional blockages that the patients consciousness imposes on him as a response to internal conflicts.
AD is characterized by a progressive weakening process, with memory disturbances being the earliest and most common manifestation of the disease. A few years after the onset of the disease, the disorders of praxis, speech, counting, writing, orientation, and recognition are systematically added, patients may have acute psychotic episodes, epileptic seizures, various extrapyramidal symptoms. There are a weakening of memory, especially short-term memory, up to a loss of the ability to navigate in simple everyday situations; emotional, cognitive, and motor function disorders (Lanctôt et al., 2017). AD, gradually progressing, transforms the still physically strong enough elderly into helpless persons with disabilities, unable to serve themselves and to require constant care from others. ASD includes the general symptoms that can be attributed to any particular type of disorder group (Constantino & Charman, 2016). These are the inability to initiate and maintain interpersonal interactions, limited interests, and repetitive, monotonous actions. Patients with autism spectrum disorders experience communication difficulties. They are unable to start and continue the dialogue, to get close to people, to empathize, to share emotions, to involve others in their ideas.
Conclusion
In conclusion, it is essential to reiterate that research into the mechanisms of neurodegenerative disease formation can significantly help in drug discovery and prevention in the developmental stages. Two opposing diseases have been considered in this paper: Alzheimers, which affects adults, and ASD, which is specific to children. The factors that form each of these diseases reveal similarities but differ at the same time. There are both experimentally proven theories of disease origin and unscientific assumptions based on environmental factors and psychosomatics. Since AD and ASD are related to diseases that affect the patients brain function, their symptoms are similar they are problems with attitudes and communication. It is erroneous to believe that the conditions described above are thoroughly studied: research continues, and new hypotheses are made. The future of medicine is likely to focus on a more detailed analysis of the genome to detect predispositions to disease in the embryonic stages of human development.
References
Alexiou, A., Soursou, G., Yarla, N. S., & Ashraf, G. M. (2018). Proteins commonly linked to autism spectrum disorder and Alzheimers disease. Current Protein and Peptide Science, 19(9), 876-880.
Alzheimers Association. (2018). 2018 Alzheimers disease facts and figures. Alzheimers & Dementia, 14(3), 367-429.
Constantino, J. N., & Charman, T. (2016). Diagnosis of autism spectrum disorder: Reconciling the syndrome, its diverse origins, and variation in expression. The Lancet Neurology, 15(3), 279-291.
Ecker, C., Bookheimer, S. Y., & Murphy, D. G. (2015). Neuroimaging in autism spectrum disorder: Brain structure and function across the lifespan. The Lancet Neurology, 14(11), 1121-1134.
Healy, D. G., Falchi, M., OSullivan, S. S., Bonifati, V., Durr, A., Bressman, S.,& Ferreira, J. J. (2008). Phenotype, genotype, and worldwide genetic penetrance of LRRK2-associated Parkinsons disease: A case-control study. The Lancet Neurology, 7(7), 583-590.
Kas, M. J., Glennon, J. C., Buitelaar, J., Ey, E., Biemans, B., Crawley, J.,& Noldus, L. P. (2014). Assessing behavioural and cognitive domains of autism spectrum disorders in rodents: Current status and future perspectives. Psychopharmacology, 231(6), 1125-1146.
Lanctôt, K. L., Amatniek, J., Ancoli-Israel, S., Arnold, S. E., Ballard, C., Cohen-Mansfield, J.,& Osorio, R. S. (2017). Neuropsychiatric signs and symptoms of Alzheimers disease: New treatment paradigms. Alzheimers & Dementia: Translational Research & Clinical Interventions, 3(3), 440-449.
Lord, C., Cook, E. H., Leventhal, B. L., & Amaral, D. G. (2000). Autism spectrum disorders. Neuron, 28(2), 355-363.
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