scholarly journals A derived mechanism of nervous system functions shows features capable to have evolved and provides a testable explanation for age-related neurodegeneration

Author(s):  
Kunjumon I Vadakkan

By viewing memories as first-person internal sensations, it was possible to derive a potential mechanism of nervous system functions. Accordingly, a spectrum inter-postsynaptic (inter-dendritic spine) functional LINKs (IPLs) are the key structural changes responsible for encoding learning-changes in physiological time-scales of milliseconds that can be retained for different lengths of time and can be used for inducing first-person inner sensation of memory. The objective of this study was to examine a) where preconditions existed for an accident to trigger sparking of internal sensations, b) what conditions might have promoted the formation and selection of IPLs, and c) how the synaptically-connected neuronal circuitry accommodated the formation of IPLs through the simple steps of variations and selection. Sequence of events during the development of the nervous system was examined for the feasible sequence of steps that led to the formation of IPLs and optimization of the system. A stage of significant spine loss and neuronal death during the early stages of development indicate about a corresponding stage of inter-spine fusion that led to neuronal loss during evolution. When the generation of internal sensations by the IPLs started to become advantageous to the system, it started preserving the circuitry by developing an adaptation to prevent inter-spine fusion. This can be achieved only if a stage of transient inter-neuronal inter-spine fusion "turn on" certain mechanism to prevent the intermediate stage of inter-spine hemifusion from progressing to fusion. In summary, the derived IPL mechanism is capable to have evolved. An adaptation to prevent IPL hemifusion from progressing to fusion is a likely evolutionary adaptation. Since the IPL mechanism is utilized during every event of learning, any age-related factors that weaken the maintenance of this adaptation to prevent IPL fusion can lead to neurodegeneration.

2019 ◽  
Author(s):  
Kunjumon I Vadakkan

By viewing memories as first-person internal sensations, it was possible to derive a potential mechanism of nervous system functions. Accordingly, a spectrum inter-postsynaptic (inter-dendritic spine) functional LINKs (IPLs) are the key structural changes responsible for encoding learning-changes in physiological time-scales of milliseconds that can be retained for different lengths of time and can be used for inducing first-person inner sensation of memory. The objective of this study was to examine a) where preconditions existed for an accident to trigger sparking of internal sensations, b) what conditions might have promoted the formation and selection of IPLs, and c) how the synaptically-connected neuronal circuitry accommodated the formation of IPLs through the simple steps of variations and selection. Sequence of events during the development of the nervous system was examined for the feasible sequence of steps that led to the formation of IPLs and optimization of the system. A stage of significant spine loss and neuronal death during the early stages of development indicate about a corresponding stage of inter-spine fusion that led to neuronal loss during evolution. When the generation of internal sensations by the IPLs started to become advantageous to the system, it started preserving the circuitry by developing an adaptation to prevent inter-spine fusion. This can be achieved only if a stage of transient inter-neuronal inter-spine fusion "turn on" certain mechanism to prevent the intermediate stage of inter-spine hemifusion from progressing to fusion. In summary, the derived IPL mechanism is capable to have evolved. An adaptation to prevent IPL hemifusion from progressing to fusion is a likely evolutionary adaptation. Since the IPL mechanism is utilized during every event of learning, any age-related factors that weaken the maintenance of this adaptation to prevent IPL fusion can lead to neurodegeneration.


2019 ◽  
Author(s):  
Kunjumon I Vadakkan

By viewing memories as first-person internal sensations, it was possible to derive a potential mechanism of nervous system functions. Accordingly, a spectrum inter-postsynaptic (inter-dendritic spine) functional LINKs (IPLs) are the key structural changes responsible for encoding learning-changes in physiological time-scales of milliseconds that can be retained for different lengths of time and can be used for inducing first-person inner sensation of memory. The objective of this study was to examine a) where preconditions existed for an accident to trigger sparking of internal sensations, b) what conditions might have promoted the formation and selection of IPLs, and c) how the synaptically-connected neuronal circuitry accommodated the formation of IPLs through the simple steps of variations and selection. Sequence of events during the development of the nervous system was examined for the feasible sequence of steps that led to the formation of IPLs and optimization of the system. A stage of significant spine loss and neuronal death during the early stages of development indicate about a corresponding stage of inter-spine fusion that led to neuronal loss during evolution. When the generation of internal sensations by the IPLs started to become advantageous to the system, it started preserving the circuitry by developing an adaptation to prevent inter-spine fusion. This can be achieved only if a stage of transient inter-neuronal inter-spine fusion "turn on" certain mechanism to prevent the intermediate stage of inter-spine hemifusion from progressing to fusion. In summary, the derived IPL mechanism is capable to have evolved. An adaptation to prevent IPL hemifusion from progressing to fusion is a likely evolutionary adaptation. Since the IPL mechanism is utilized during every event of learning, any age-related factors that weaken the maintenance of this adaptation to prevent IPL fusion can lead to neurodegeneration.


2019 ◽  
Author(s):  
Kunjumon I Vadakkan

By viewing memories as first-person internal sensations, it was possible to derive a potential mechanism of nervous system functions. Accordingly, a spectrum inter-postsynaptic functional LINKs (IPLs) are the key structural changes responsible for encoding learning-changes in physiological time-scales of milliseconds that can be retained for variable lengths of time. The inter-spine interaction that lead to the formation of IPLs was examined for its feasibility to have evolved through the simple steps of variation and selection. A stage of significant spine and neuronal loss during the early stages of development indicates that a corresponding stage of IPL fusion that led to neuronal loss during evolution. In the surviving cells is expected that a mechanism for stabilizing IPLs for the rest of life was triggered. This sequence of events can be achieved if the initial stage of transient inter-neuronal inter-spine fusion can trigger the lifelong expression of specific proteins that can stabilize the intermediate stage of inter-spine hemifusion. This is supported by the presence of proteins within the spines that arrest fusion between the spines. Since IPL mechanisms are expected to be utilized during every event of learning, any defect in the continued expression of proteins that stabilizes IPLs at the stage of hemifusion can lead to age-related neurodegeneration.


2020 ◽  
Vol 13 (2) ◽  
pp. 136-152
Author(s):  
Kunjumon I. Vadakkan

Background: Solving the nervous system requires understanding how it generates inner sensations of "mind" within it. It was possible to derive a hypothesis of brain functions where the formation of a spectrum inter-postsynaptic (inter-spine) functional LINKs (IPLs) are the key structural changes responsible for encoding at the time of learning and are used for inducing the inner sensation of memory, both taking place at millisecond timescales. Since stages of ontogeny reflect possible stages of evolution, it is possible to examine whether IPLs have features of an evolved mechanism. Objective: To examine whether 1) IPLs have features of an evolved mechanism, 2) significant neuronal death during ontogeny leads to evolutionary adaptations for preventing cell death among the surviving neurons, and 3) loss of these adaptations lead to cellular changes that can cause agingrelated neurodegeneration. Methods: Key milestone changes of the ontogeny of the nervous system were examined to test whether they match with a feasible sequence of steps that lead to the formation of IPLs. Results: Several developmental stages can explain a probable sequence of events that lead to IPL formation among synaptically-connected neurons. When internal sensations generated by the IPLs started providing survival advantage, evolution has started preserving the IPL circuitry. A stage of inter-spine fusion possibly leads to a) significant neuronal death during the early stages of development, and b) trigger an adaptation in the surviving cells to stabilize and prevent the IPLs from undergoing fusion. Since there are no irreversible steps for maintaining the stability of IPLs, agingrelated factors may destroy the adaptation mechanism and destabilize the IPLs predisposing them to cause neurodegeneration. Conclusion: The derived testable IPL mechanism that can explain nervous system functions is capable to have evolved. An adaptation to prevent IPL hemifusion from progressing to fusion is likely the last stage of nervous system evolution. Since the IPL mechanism is utilized during every event of learning, any aging-related factors that can weaken this adaptation can cause IPL fusion and lead to neurodegeneration.


2009 ◽  
Vol 9 ◽  
pp. 1061-1071 ◽  
Author(s):  
David R. Brown

Microglia play a curious role in the nervous system. Their role is intrinsically protective and supportive, but during neurodegenerative disease, it is well established that microglia play a significant role in the initiation of neuronal death. Microglia, like neurons, show age-related changes that could potentially alter their behavior. While extreme changes to a large population of microglia cause dramatic neuronal loss in neurodegeneration, during normal aging, subtle changes not unlike those seen in the disease state could potentially contribute to a more gradual neuronal loss that could contribute to the cognitive decline seen in the aging population. This review provides illustrations of what is known about the role of microglia in neurodegeneration and makes suggestions about the role of microglia in age-related changes to the brain.


Author(s):  
В. А. Сальников ◽  
Е. М. Ревенко

В статье рассматривается соотношение возрастных и индивидуально-типологических особенностей в развитии двигательных способностей в системе физического воспитания и спортивной деятельности. Отмечается, что на рубеже 60 - 80-х гг. прошлого века получен обширный материал относительно развития двигательных способностей, где возраст выступал в качестве интегрального показателя. В исследованиях последующего периода явно обозначилось, что возрастной критерий не позволяет в полной мере раскрыть закономерности развития двигательных способностей, а возраст как таковой не может отражать какого бы то ни было стандартного процесса развития. Утверждается, что возрастные особенности наиболее полно могут быть представлены в контексте целостного процесса индивидуального развития человека. Результаты исследования показали, что в процессе взросления развитие двигательных способностей связано со свойствами нервной системы, при этом выявленные связи существенно различаются в различные возрастные периоды. Также существенно различаются связи, с одной стороны, исходных уровней проявлений двигательных способностей, с другой, - темпов их прироста с типологическими свойствами нервной системы в отдельно взятых возрастных периодах. Наличие устойчивых взаимосвязей уровней проявлений и темпов прироста двигательных способностей со свойствами нервной системы свидетельствует об индивидуальных траекториях развития двигательных проявлений в онтогенезе. Знание последних позволит индивидуализировать образовательный и тренировочный процессы. Динамика развития двигательных способностей определяется совокупностью типологических особенностей проявления свойств нервной системы - типологическим комплексом. The article deals with the correlation of age and individual typological features in the development of motor abilities in the system of physical education and sports activities. It is noted that at the turn of the 60 - 80s of the last century, extensive material was obtained on the development of motor abilities, where age was an integral indicator. In studies of the subsequent period, it was clearly indicated that the age criterion does not allow to fully reveal the laws of development of motor abilities, and age as such cannot reflect any standard development process. It is argued that age-related features can be most fully represented in the context of a holistic process of individual human development. The results of the study showed that in the process of growing up, the development of motor abilities is associated with the properties of the nervous system, while the revealed connections differ significantly in different age periods. There are also significant differences in the relationship, on the one hand, of the initial levels of motor abilities, and, on the other hand, the rate of their growth with the typological properties of the nervous system in individual age periods. The presence of stable relationships between the levels of manifestations and the rate of growth of motor abilities with the properties of the nervous system indicates individual trajectories of development of motor manifestations in ontogenesis. Knowledge of the latter will allow you to individualize the educational and training processes. Dynamics of development of motor abilities is determined by a set of typological features of the manifestation of the properties of the nervous system - a typological complex.


2018 ◽  
Vol 2 (1) ◽  
pp. 01-03
Author(s):  
Ruth Angale

Mitochondria are cytoplasmic organelles responsible for life and death. Extensive evidence from animal and clinical studies suggests that mitochondria play a critical role in aging, cancer, diabetes and neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. Several lines of research suggest that mitochondrial oxidative damage is an important cellular change in most late-onset neurodegenerative diseases. Further, emerging evidence suggests that structural changes in mitochondria, including increased mitochondrial fragmentation and decreased mitochondrial fusion, are critical factors associated with mitochondrial dysfunction and cell death in aging and age-related diseases. In addition, epigenetic factors and lifestyle activities may contribute to selective disease susceptibility for each of these diseases. This paper discusses research that has elucidated features of mitochondria that are associated with cellular dysfunction in aging and neurodegenerative diseases. This paper also discusses mitochondrial abnormalities and potential mitochondrial therapeutics in AD. Alzheimer's disease (AD) is characterized by neuronal loss and gradual cognitive impairment. AD is the leading cause of dementia worldwide and the incidence is increasing rapidly, with diagnoses expected to triple by the year 2050. Impaired cholinergic transmission is a major role player in the rapid deterioration associated with AD, primarily as a result of increased acetylcholinesterase (AChE) in the AD brain, responsible for reducing the amount of acetylcholine (ACh). Current drug therapies, known as AChE inhibitors (AChEIs), target this heightened level of AChE in an attempt to slow disease progression. AChEIs have only showed success in the treatment of mild to moderate AD symptoms, with the glutamate inhibitor memantine being the most common drug prescribed for the management of severe AD.


Author(s):  
K. Kovacs ◽  
E. Horvath ◽  
J. M. Bilbao ◽  
F. A. Laszlo ◽  
I. Domokos

Electrolytic lesions of the pituitary stalk in rats interrupt adenohypophysial blood flow and result in massive infarction of the anterior lobe. In order to obtain a deeper insight into the morphogenesis of tissue injury and to reveal the sequence of events, a fine structural investigation was undertaken on adenohypophyses of rats at various intervals following destruction of the pituitary stalk.The pituitary stalk was destroyed electrolytically, with a Horsley-Clarke apparatus on 27 male rats of the R-Amsterdam strain, weighing 180-200 g. Thirty minutes, 1,2,4,6 and 24 hours after surgery the animals were perfused with a glutaraldehyde-formalin solution. The skulls were then opened and the pituitary glands removed. The anterior lobes were fixed in glutaraldehyde-formalin solution, postfixed in osmium tetroxide and embedded in Durcupan. Ultrathin sections were stained with uranyl acetate and lead citrate and investigated with a Philips 300 electron microscope.


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