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What Is The Role Of Myelin Sheath

Although Alois Alzheimer described the breakdown of myelin in Alzheimer’s disease (AD) as early as 1911, his observation has escaped the attention of researchers since then. Alzheimer’s disease is considered a gray matter disease; however, recent evidence suggests that myelin dysfunction may play an important role in the pathogenesis of AD. The classic neuropathological changes in AD, e.g. the accumulation of Aβ 42 and the presence of neurofibrillary tangles, are responsible for neuronal loss, but can also cause the death of oligodendrocytes and myelin damage. There is also evidence that myelin pathology may even precede Aβ and tau lesions in AD. The state of the art does not allow us to determine whether myelin damage is primary or secondary in AD phenomena. The article presents an overview of the current knowledge on the role of myelin in the pathogenesis of AD and its interaction with Aβ and tau pathologies.

Cns Myelin Sheath Lengths Are An Intrinsic Property Of Oligodendrocytes

Alzheimer’s disease (AD) is known to cause some behavioral changes, such as accumulation of amyloid plaques, intra-neuronal presence of neurofibrillary tangles, glial hypertrophy, and neuronal death [1-3]. The disease is associated with neuronal damage; however, there is evidence that myelin fibers are also damaged in AD. Myelin pathology has not yet been studied in patients with AD, although Alois Alzheimer described myelin disruption in AD as early as 1911 [4, 5]. It is not known why the phenomenon of myelin deficiency has been forgotten for more than 100 years. The 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 have also been observed in the brains of AD patients [6-9].

The myelin sheath is a lipid-rich, multilamellar membrane that is wrapped around the axon. Myelin dysfunction has been suggested to cause neuronal dysfunction and cognitive decline. Myelin is necessary for propagation through the axon. In addition, there is evidence from neuroimaging and human brain data analysis that myelin damage may be associated with the presence of amyloid β (Aβ) plaques and tau hyperphosphorylation, which are found in AD [6, 7, 10, 11]. Interestingly, the prevalence of AD pathology shows earlier myelination [12]. Later myelinated brain regions, such as the temporal and frontal lobes, develop AD pathology before the onset of myelinating regions, mainly the motor and sensory systems, which may be present in AD until the late stages of the disease [13- 16]. Some studies also suggest that AD is a developmental disease, which can only occur once myelination is complete [13, 14]. One recent study also revealed a defect in the biosynthesis of myelin lipids in the early stages of AD, which significantly contributes to the deterioration of synaptic function and cognitive decline [16]. What is interesting, the damage to the brain tissue is the same as the brain. Tumor Tumor Tumor Tumor Tumor Tumor Tumor Tumor Tumor Tumor Tumor Tumor Tumor Tumor Tumor Tumor Aberrant brain cell dysfunction has been implicated in AD [ 16 ]. The above data suggest that AD may be a demyelination disorder. Over time, myelin damage can contribute to synaptic dysfunction and cognitive decline. The article presents the current knowledge about the role of myelin in AD, and its interaction with amyloid depositions in the brain of AD patients.

Myelin is wrapped around the axons of neurons and forms structures called nodes of Ranvier where action potentials are generated, to propagate along myelinated axons [17]. Conduction speed along myelinated axons not only depends on the axonal diameter, but is also regulated by the number and geometry of the nodes of Ranvier [17]. Myelin damage 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 hippocampus of rats treated with experimental autoimmune encephalitis (EAE) [18, 19]. This study 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 axonal inhibitors sprouting, which is important. for the formation of synapses [20]. But in addition to these proteins, many other factors can contribute to the poor structure and function of synapses. As a result of demyelination, dysfunction of axonal transport may occur. Proper myelin activity has a beneficial effect on neuronal function. Myelin damage can impair neuronal function, as myelin supports axonal survival. Oligodendrocytes are capable of secreting 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 survival neuronal [21]-23]. Clinically this translates into cognitive impairment, as various myelination disorders cause cognitive decline.

The Architecture And Molecular Composition Of Myelin In The Cns….

Data from experimental animal models of AD also suggest that there may be extensive damage in the vicinity of Aβ plaques in the neocortex [ 10 , 11 , 24 ]. Schmued et al. there was evidence for complete disruption of myelinated fibers passing through Aβ plaques or adjacent plaques in the hippocampal region in rats [24]. Therefore, various data from animal models show that demyelination can lead to neuronal damage and axonal degeneration. Both of these factors can contribute to the cognitive deficits seen in AD.

Data from animal models also provide evidence for an interaction between tau pathology and myelin degeneration. Myelin damage has been found to occur before the formation of Aβ plaques and neurofibrillary tangles in the brains of murine models of AD [ 25 , 26 ]. Defects in myelin biosynthesis have been found in AD subjects even in the early stages of the disease, e.g. Braak Stage I/II in temporal lobes, which also confirmed that myelin degeneration precedes amyloid pathology [16]. Couttas et al. a significant decrease was observed in the activity of ceramide synthase 2, which is responsible for the synthesis of long-chain ceramides of the lipids of the myelin sheath. This finding may support the hypothesis that demyelination may have a driving effect in AD disease [16].

Myelin damage is probably an early factor in the pathology of AD, which precedes the characteristic 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 found in some demyelinating diseases [28]. It is not yet known whether myelin damage actually causes the development of AD.

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

Cns Myelination Requires Vamp2/3 Mediated Membrane Expansion In Oligodendrocytes

Data from animal models have shown that the expression of myelin basic protein (MBP), which is an important component of the myelin sheath, is significantly higher in rats that have received training in learning tasks than in rats that have not received the same this training is not, and the level of MBP is directly related with the learning rate [32, 33]. What is interesting, in adult mice that have to learn motor skills, the occurrence of new Oligodonences and Myelin Colorsum [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 age-related cognitive decline is associated with changes in white matter [37], which may be caused by marked degeneration and loss of oligodendrocytes. Age-related changes in white matter integrity are associated with cognitive decline in healthy older adults [38]. Another thing to note is that there is evidence that memory training can increase genetic integrity in the elderly and at the same time improve their cognitive abilities [39]. To conclude, aging-related myelin damage may contribute to cognitive decline in healthy older adults (Figure 1).

The role of myelin in cognition. The picture shows the consequences of myelin damage for cognition. Myelin is responsible for transmitting 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 the transport of trophic factors including fast axonal transport.

The amyloid hypothesis must be confirmed, as an adjustment

Myelin Sheath: What They Are, Their Function, & Damage

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