CRIMEA STATE MEDICAL UNIVERSITY NAMED AFTER S.I. GEORGIEVSKY презентация

CRIMEA STATE MEDICAL UNIVERSITY NAMED AFTER S.I. GEORGIEVSKY Topic:- Phylogenetic disorders of brain By:- Tiwari Shivani Group:- 191A Guided by :- Zhukova Anna

PHYLOGENETIC DISORDERS OF BRAIN

CONTENT PHYLOGENESIS BRAIN EVOLUTION OF THE BRAIN Alzheimer's disease Parkinson's disease Reference

PHYLOGENESIS the evolutionary development and diversification of a species or group of organisms, or of a particular feature of an organism. Phylogentics:- relating to the evolutionary development and diversification of a species or group of organisms, or of a particular feature of an organism.

BRAIN The brain is one of the largest and most complex organs in the human body. It is made up of more than 100 billion nerves that communicate in trillions of connections called synapses. The brain is made up of many specialized areas that work together: • The cortex is the outermost layer of brain cells. The adult human brain weighs on average about 1.5 kg (3.3 lb). In men the average weight is about 1370 g and in women about 1200 g. The volume is around 1260 cm3 in men and 1130 cm3 in women, although there is substantial individual variation.

As a number, a “petabyte” means 1024 terabytes or a million gigabytes, so the average adult human brain has the ability to store the equivalent of 2.5 million gigabytes digital memory. As a number, a “petabyte” means 1024 terabytes or a million gigabytes, so the average adult human brain has the ability to store the equivalent of 2.5 million gigabytes digital memory. Average weight 1400 grams

EVOLUTION OF THE BRAIN One of the prominent ways of tracking the evolution of the human brain is through direct evidence in the form of fossils. The evolutionary history of the human brain shows primarily a gradually bigger brain relative to body size during the evolutionary path from early primates to hominids and finally to Homo sapiens. On average, the size of primates' brains is nearly double what is expected for mammals of the same body size. Across nearly seven million years, the human brain has tripled in size, with most of this growth occurring in the past two million years

Alzheimer's disease Alzheimer's disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks. The study finds evidence that 50,000 to 200,000 years ago, natural selection drove changes in six genes involved in brain development.

Approaching the disease from an evolutionary standpoint may help in understanding the root cause of human vulnerability to the disease. Approaching the disease from an evolutionary standpoint may help in understanding the root cause of human vulnerability to the disease. AD is very common in humans and extremely uncommon in other mammals, which suggests that the genetic changes underlying the alterations in cerebral structure or function that have taken place over the course of the evolution of the genus Homo have left specific neurons in the human brain particularly vulnerable to factors which trigger the disease.

Neurons in certain association areas of the human brain retain juvenile characteristics into adulthood, such as the increased expression of genes related to synaptic activity and plasticity, incomplete myelination and elevated aerobic metabolism, which can cause an increase in oxidative stress in these neurons. Oxidative stress can cause myelin breakdown and epigenetic changes in the promoter region of genes related to synaptic plasticity, reducing their expression. These changes may in some cases induce hyperphosphorylation of tau and β-amyloid deposits, which are characteristic of AD. The adaptation of humans to the cognitive niche probably required an increase in synaptic plasticity and activity and neuronal metabolism in neurons in areas related to certain cognitive functions such as autobiographical memory, social interaction and planning. Neurons in certain association areas of the human brain retain juvenile characteristics into adulthood, such as the increased expression of genes related to synaptic activity and plasticity, incomplete myelination and elevated aerobic metabolism, which can cause an increase in oxidative stress in these neurons. Oxidative stress can cause myelin breakdown and epigenetic changes in the promoter region of genes related to synaptic plasticity, reducing their expression. These changes may in some cases induce hyperphosphorylation of tau and β-amyloid deposits, which are characteristic of AD. The adaptation of humans to the cognitive niche probably required an increase in synaptic plasticity and activity and neuronal metabolism in neurons in areas related to certain cognitive functions such as autobiographical memory, social interaction and planning.

The cost of these changes may have been the brain's increased vulnerability to factors which can trigger AD. This vulnerability may have resulted from the evolutionary legacies that have occurred over the course of the evolution of the human brain, making AD a possible example of antagonistic pleiotropy. The evolutionary approach allows apparently unrelated data from different disciplines to be combined in a manner that may lead to an improved understanding of complex diseases such as Alzheimer's. The cost of these changes may have been the brain's increased vulnerability to factors which can trigger AD. This vulnerability may have resulted from the evolutionary legacies that have occurred over the course of the evolution of the human brain, making AD a possible example of antagonistic pleiotropy. The evolutionary approach allows apparently unrelated data from different disciplines to be combined in a manner that may lead to an improved understanding of complex diseases such as Alzheimer's.

Parkinson's disease Parkinson's disease is a progressive nervous system disorder that affects movement. Symptoms start gradually, sometimes starting with a barely noticeable tremor in just one hand. Tremors are common, but the disorder also commonly causes stiffness or slowing of movement.

There are two central premises to this evolutionary view of Parkinson disease (PD). First, PD is a specific human disease. Second, the prevalence of PD has increased over the course of human history. Several lines of evidence may explain why PD appears to be restricted to the human species. The major manifestations of PD are the consequence of degeneration in the dopamine-synthesizing neurons of the mesostriatal neuronal pathway. It is of note the enormous expansion of the human dopamine mesencephalic neurons onto the striatum compared with other mammals. Hence, an evolutionary bottle neck was reached with the expansion of the massive nigrostriatal axonal arborization. This peculiar nigral overload may partly explain the selective fragility of the human dopaminergic mesencephalic neurotransmission and the unique presence of PD in humans. There are two central premises to this evolutionary view of Parkinson disease (PD). First, PD is a specific human disease. Second, the prevalence of PD has increased over the course of human history. Several lines of evidence may explain why PD appears to be restricted to the human species. The major manifestations of PD are the consequence of degeneration in the dopamine-synthesizing neurons of the mesostriatal neuronal pathway. It is of note the enormous expansion of the human dopamine mesencephalic neurons onto the striatum compared with other mammals. Hence, an evolutionary bottle neck was reached with the expansion of the massive nigrostriatal axonal arborization. This peculiar nigral overload may partly explain the selective fragility of the human dopaminergic mesencephalic neurotransmission and the unique presence of PD in humans.

On the other hand, several facts may explain the increasing prevalence of PD over the centuries. The apparently low prevalence of PD before the twentieth century may be related to the shorter life expectancy and survival compared to present times. In addition, changes in lifestyle over the course of human history might also account for the increasing burden of PD. Our hunter-gatherers ancestors invested large energy expenditure on a daily basis, a prototypical physical way of life for which our genome remains adapted. Technological advances have led to a dramatic reduction of physical exercise. Since the brain release of neurotrophic factors (including brain-derived neurotrophic factor) is partially exercise related, the marked reduction in exercise may contribute to the increasing prevalence of PD. On the other hand, several facts may explain the increasing prevalence of PD over the centuries. The apparently low prevalence of PD before the twentieth century may be related to the shorter life expectancy and survival compared to present times. In addition, changes in lifestyle over the course of human history might also account for the increasing burden of PD. Our hunter-gatherers ancestors invested large energy expenditure on a daily basis, a prototypical physical way of life for which our genome remains adapted. Technological advances have led to a dramatic reduction of physical exercise. Since the brain release of neurotrophic factors (including brain-derived neurotrophic factor) is partially exercise related, the marked reduction in exercise may contribute to the increasing prevalence of PD.

SYMPTOMS

Reference Evans DA, Funkenstein HH, Albert MS, Scherr PA, Cook NR, Chown MJ, Hebert LE, Hennekens CH, Taylor JO. Prevalence of Alzheimer's disease in a community population of older persons: higher than previously reported. JAMA. 1989;262:2551–6. [PubMed] [Google Scholar] Kalia LV, Lang AE. Parkinson’s disease. Lancet (2015) 386:896–912.10.1016/S0140-6736(14)61393-3 - DOI - PubMed Wikipedia

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