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What Is The Function Of Myelin Sheath In A Neuron
Although Alois Alzheimer described the Myelin disorder in Alzheimer’s disease (AD) as early as 1911, his finding has since escaped the attention of researchers. Alzheimer’s disease has largely been considered a gray matter disorder; nevertheless, recent evidence suggests that myelin impairment 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 can also cause oligodendrocyte death and myelin damage. There is also evidence that myelin pathology may even precede Aβ and tau pathologies in AD. The state of the art does not allow us to determine whether myelin damage is primary or secondary damage in AD patients. The article presents a review of current knowledge on the role of myelin in AD pathology and its interactions with Aβ and tau pathologies.
Myelin Damaged By Multiple Sclerosis Could Be Repaired By Reducing Levels Of An Enzyme
Alzheimer’s disease (AD) is known to lead to some well-defined pathological changes, such as extracellular accumulation of amyloid plaques, intraneuronal presence of neurofibrillary tangles, glial hypertrophy and neuronal death [1–3]. The disease is mainly associated with damage to neurons; however, there is evidence that myelin fibers are also damaged in AD. The pathology of myelin in AD patients has not yet been widely studied, although Alois Alzheimer described a myelin disorder in AD as early as 1911 [ 4 , 5 ]. It is not clear why the phenomenon of myelin damage has been forgotten for more than 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, but oligodendroglial degeneration and myelin damage have also been observed in the brains of AD patients [6–9].
The Myelin Sheath is a lipid-rich multilamellar membrane wrapped around axons. Myelin damage is thought to lead to neuronal dysfunction and cognitive decline. Myelin is necessary for the propagation of impulses along axons. In addition, there is evidence from neuronal imaging and post-mortem studies of human brains that myelin damage may be associated with the presence of amyloid β (Aβ) plaques and tau hyperphosphorylation found in AD [ 6 , 7 , 10 , 11 ]. Interestingly, the spread of AD pathology mirrors the pattern of myelination in the reverse direction [12]. Later myelinated brain regions, such as the temporal and frontal lobes, develop AD pathology before early myelinated regions, especially the motor and sensory systems, which may remain intact in AD until very late stages of the disease [13–16]. Some studies also suggest that AD is a developmental disorder that may only appear when myelination is complete [13, 14]. One recent study also revealed a defect in the biosynthesis of myelin lipids in the preclinical phase of AD, which significantly contributes to deterioration of synaptic function and cognitive decline [16]. Interestingly, impaired myelin sheath formation appears to even precede neurofibrillary tangle pathology in AD patients, suggesting that myelin damage may be the first neuropathological abnormality in AD [16]. The above data suggest that AD may be a demyelinating disorder. Over time, myelin damage can contribute 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 deposition 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 and then propagate along the myelinated axons [17]. The speed of translation along myelinated axons depends not only on the diameter of the axons, but is also regulated by the number and geometry of the nodes of Ranvier [17]. Myelin disorders can affect the transmission of action potentials in neurons. Data from animal neuropathological studies have shown reduced synaptic staining and impaired synaptic transmission in the demyelinated hippocampus of mice with experimental autoimmune encephalitis (EAE) [ 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, act as inhibitors of axon sprouting, which is important for formation of synapses [20]. But in addition to these proteins, many other factors can contribute to the defective structure and function of synapses. Demyelination can lead to dysfunction of axonal transport. The proper functioning of myelin also has a beneficial effect on the functioning of neurons. Damage to myelin can impair neuronal function, as myelin supports the survival of axons. Oligodendrocytes have the ability 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 have a beneficial effect on neuronal survival [21]. –23]. Clinically, this translates into deterioration of cognition, as various myelination disorders cause cognitive decline.
Multiple Sclerosis And Myelin Sheath Breakdown Stock Illustration
Data from experimental animal models of AD also suggest that focal demyelination can be found primarily near Aβ plaques in the neocortex [ 10 , 11 , 24 ]. Schmued et al. found evidence for complete disruption of myelinated fibers passing through or near Aβ plaques in the hippocampal region of rats [24]. Thus, various data from animal models suggest that demyelination can cause degeneration of neurons and axons. Both factors may underlie the cognitive impairment observed in AD.
Data from animal models also demonstrate an interaction between tau pathology and myelin damage. Myelin damage has been found to occur before the deposition of Aβ plaques and neurofibrillary tangles in the brains of mouse models of AD [ 25 , 26 ]. A defect in myelin biosynthesis has been identified in AD subjects already in the very early, preclinical stages of the disease, e.g. Braak stage 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 belonging to the lipids of the myelin sheath. This finding may support the hypothesis that demyelination may influence the pathogenesis of AD [16].
Myelin damage is likely to be an early phenomenon in AD pathology, preceding the onset of typical pathological changes such as Aβ plaques and neurofibrillary tangles. Interestingly, there is also evidence that tau protein hyperphosphorylation can 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 detected in other demyelinating disorders [28]. It is still not clear whether myelin damage really initiates the onset of AD pathology.
The development of myelin progresses during childhood and adolescence, until adulthood [29]. Myelination of the central nervous system is completed in different parts of the brain at different time points. In humans, the development of myelin in the corpus callosum, unlike the formation of neurons, is completed only in the second decade of life [30], and in the frontal lobes only at about the age of forty [31]. . Myelination is directly related to the development of cognitive and motor functions.
Anatomy Qa: Myelin And Neurilemma Sheaths
Data from animal models show that the expression of myelin basic protein (MBP), an important compound of the myelin sheath, is significantly higher in rats that have been trained in learning tasks than in rats that have not received such training, and MBP levels is directly related to the level of learning [32, 33]. Interestingly, in adult mice that had to learn complex motor skills, new oligodendrocytes and myelin were found in the corpus callosum [34, 35].
The integrity of the myelin sheath decreases with age, and with it 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 age-related cognitive decline is associated with changes in 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 elderly subjects [38]. It is worth noting that there is evidence that memory training can increase white matter integrity in older people while improving their cognitive ability [39]. In conclusion, aging-related myelin damage may contribute to cognitive decline in healthy elderly subjects (Figure 1).
The role of myelin in cognition. The figure shows the results 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 functioning. Myelin damage impairs neuronal function, increases neuronal energy consumption, and reduces transport of trophic factors and fast axonal transport
The amyloid hypothesis should be tested as a correlation
Ms Related Study Shows Inhibiting Enzyme Reverses Myelin Damage
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