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What Is The Function Of Myelin Sheath

Although Alois Alzheimer described the breakdown of myelin in Alzheimer’s disease (AD) in 1911, his observation has since eluded researchers. Alzheimer’s disease is largely considered a gray disease; However, recent evidence suggests that myelin deficiency may play an important role in AD pathology. Classic neuropathological changes in AD, e.g. the accumulation of aggregated Aβ 42 and the presence of neurofibrillary tangles are responsible for neuronal loss, but they can also cause the death of oligodendrocytes and myelin damage. There is also evidence that myelin pathology may precede Aβ and tau pathologies in AD. The state of the art does not allow us to determine whether myelin damage is a primary or secondary lesion in AD subjects. The article presents an overview of current knowledge on the role of myelin in AD pathology and its interactions with Aβ and tau pathologies.

Myelin Sheath: Diagram And Function

Alzheimer’s disease (AD) is known to cause some well-characterized pathological changes, such as extracellular accumulation of amyloid plaques, intra-neuronal presence of neurofibrillary tangles, glial hypertrophy, and neuronal death [1-3]. The disease is mainly associated with neuronal damage; however, there is evidence that myelin fibers are also damaged in AD. Myelin pathology in patients with AD has not been extensively studied until now, although Alois Alzheimer described myelin disruption in AD as early as 1911 [ 4 , 5 ]. It is not clear why the phenomenon of myelin deficiency has been forgotten for 100 years. Classic neuropathological changes in AD, e.g. Amyloid plaque deposition and the presence of neurofibrillary tangles in the brain are responsible for neuronal damage and synapse loss, while oligodendroglial degeneration and myelin depletion have also been observed in the brains of AD patients [6-9].

The myelin sheath is a lipid-rich, multi-lamellar membrane that wraps around axons. It is suggested that myelin deficiency leads to neuronal dysfunction and cognitive decline. Myelin is necessary for impulse propagation along axons. In addition, there is evidence from neuroimaging and recent studies of the human brain that myelin damage may be associated with the presence of amyloid β (Aβ) plaques and tau hyperphosphorylation, both of which are seen in AD [6, 7, 10, 11]. be Interestingly, the prevalence of AD pathology shows a reversed myelination pattern [12]. Later myelinated brain areas, such as the temporal and frontal lobes, AD pathology precedes early myelinated areas, especially the motor and sensory systems, which may remain intact in AD until very late stages of the disease [13–16 ]. Some studies also show that AD is a developmental disease, which occurs only after myelination is complete [13, 14]. A recent study also revealed a defect in the biosynthesis of myelin lipids in the preclinical stage of AD, which significantly contributes to the deterioration of synaptic function and cognitive decline [ 16 ]. Interestingly, impaired myelin formation in AD patients also appears to prevent the pathology of neurofibrillary tangles, suggesting that myelin damage may be the first neuropathological abnormality in AD [16]. The above data suggest that AD may be a demyelination disease. Over time, myelin damage can lead to synaptic dysfunction and cognitive decline. The article presents current knowledge on the role of myelin in AD, as well as its interactions with amyloid deposits in the brains of AD patients.

Myelin is wrapped around the axons of neurons and forms structures called nodes of Ranvier where action potentials are generated, to then be propagated along the myelinated axons [17]. The speed of conduction along myelinated axons depends not only on axonal diameter, but is also regulated by the number and geometry of nodes of Ranvier [ 17 ]. Myelin defects can affect the transmission of action potentials in neurons. Data from neuropathological animal studies in the demyelinated hippocampus of mice with experimental autoimmune encephalitis (EAE) revealed reduced synaptic staining and inhibition of synaptic transmission [ 18 , 19 ]. This finding confirms that myelin plays an important role in synaptic transmission.

In addition, proteins such as neurite outgrowth inhibitor-A (Nogo-A), myelin-associated glycoprotein (MAG), and oligodendrocyte myelin glycoprotein (MOG), which are expressed in oligodendrocytes and myelin, are important axon inhibitors. act to build synapses [20]. But in addition to these proteins, many other factors can cause the breakdown of the structure and function of synapses. As a result of demyelination, dysfunction of axonal transport occurs. Proper myelin function also has a beneficial effect on neuronal function. Myelin deficiency may impair neuronal function, as myelin supports axonal survival. Oligodendrocytes have the capacity to secrete trophic factors such as insulin-like growth factor-1 (IGF-1), glial cell-derived neurotrophic factor (GDNF), and nerve growth factor (NGF), which exert beneficial effects on neuronal survival [ 21-23]. Clinically this translates into cognitive impairment, as various myelination disorders cause cognitive impairment.

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Data from experimental animal models of AD also indicate that focal demyelination is often observed in proximity to Aβ plaques within the neocortex [ 10 , 11 , 24 ]. Schmued et al. found evidence for complete destruction of myelinated fibers passing through Aβ plaques or near plaques in the hippocampal region in rats [24]. Thus, various data from animal models suggest that demyelination may lead to neuronal and axonal degeneration. Both of these factors may underlie the cognitive impairment seen in AD.

Data from animal models also provide evidence for a link between tau pathology and myelin deficiency. Myelin damage has been found to occur before the destruction of Aβ plaques and neurofibrillary tangles in the brains of mouse models of AD [ 25 , 26 ]. A deficiency in myelin biosynthesis has been observed in AD subjects even in very early, preclinical stages of the disease, e.g. Braak phase I/II in the temporal cortex, which also confirms that myelin dysfunction precedes amyloid pathology [16]. Couttas et al. observed a significant decrease in the activity of ceramide synthase 2, which is responsible for the synthesis of very long chain ceramides associated with the lipids of the myelin sheath. This finding may support the hypothesis that demyelination may have a driving effect in the pathogenesis of AD [16].

Myelin deficiency may be an early phenomenon in AD pathology, which precedes the onset of pathological changes such as Aβ plaques and neurofibrillary tangles. Interestingly, there is also evidence that tau protein hyperphosphorylation may occur later, during the remyelination process [27]. It should be noted here that hyperphosphorylated tau protein, as a marker of axonal and neuronal loss, has also been observed in other demyelinating diseases [28]. It is still unclear whether myelin damage actually causes AD pathology.

Myelin development continues throughout childhood and adolescence, into adulthood [29]. Myelination of the central nervous system is completed at different times in different areas of the brain. In humans, the development of myelin in the corpus callosum, unlike the formation of neurons, is not complete until the second decade of life [30], and in the frontal lobes, until the age of forty [31] . Myelination is directly related to cognitive development and motor function.

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Data from animal models show that the expression of myelin basic protein (MBP), an important component of the myelin sheath, is significantly higher in mice trained in learning tasks than in untrained mice, and MBP levels are directly related to rate of learning [32, 33]. Interestingly, in older rats that had to learn complex motor skills, the appearance of new oligodendrocytes and myelin in the corpus callosum was observed [34, 35].

The integrity of the myelin sheath decreases with age, and so does the amount of myelin in the brain. Myelin content peaks in middle age and gradually declines in later years [ 14 , 36 ]. There is evidence that cognitive decline with age is related to changes in the white matter [37], which may be caused by marked demyelination and loss of oligodendrocytes. Age-related changes in white matter integrity are associated with cognitive decline in healthy older individuals [38]. A point worth noting is that there is evidence that memory training can increase white matter integrity in older people and at the same time improve their cognitive capacity [39]. In conclusion, myelin damage associated with aging may contribute to cognitive decline in healthy older people (Figure 1).

The role of myelin in cognition. The figure shows the consequences of myelin damage for cognition. Myelin is responsible for the transmission of action potentials. Myelin proteins are involved in the formation of synapses and their proper function. Myelin damage impairs neuronal function, increases energy consumption by neurons and impairs transport of trophic factors as well as rapid axonal transport.

The amyloid hypothesis needs to be verified, as does the correlation

Axon Hillock Definition And Examples

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