Memory Disorders and Alzheimer's

Memory Disorders and Alzheimer's
📌Category: Disorders, Health, Illness, Medicine, Memory
📌Words: 997
📌Pages: 4
📌Published: 10 April 2021

Instead of utilising healthy individuals, to evaluate SCT possibility of increasing memory capacity. Individuals suffering from a neurodegenerative disease like Alzheimer (AD) would be more useful.

AD is a neurodegenerative disorder resulting in a decline in memory function. To the point, individuals are unable to perform daily activities. AD achieves via its main symptom, dementia. Dementia is a syndrome made up of symptoms that result in a decline in cognitive functions(5). In 2015 29.8 million people globally had Alzheimer’s(6). This number is predicted to increase to 155 million by 2050(6). A lack of a cure is the main reason for this. Currently, there are pharmacological and immunological treatments to treat AD. Treatment only delays its progression. None can reverse the decrease in memory capacity caused by neurodegeneration.

Current treatment for AD is based, on the popular beta-amyloid (Aβ) and Tau model. This model states that the accumulation of these two proteins leads to the death of neuronal cells. Production of Aβ is due to proteolytic cleavage of Amyloid precursor protein (APP). Through the Amyloidogenic pathway, shown in the above diagram. APP is a normal protein found in cells within and outside the central nervous system (CNS). Amyloidogenic cleavage of APP is a normal pathway. Aβ produced from it, is normally cleared from the brain. Before it aggregates into plaques, and its neurotoxic functions take effect. A route used to remove Aβ is its degradation through cellular uptake. This mechanism is reduced in AD patients leading to Aβ to neurotoxic function, as it accumulates. Through interaction with neuronal proteins like fibrinogen, Aβ triggers neuroinflammation, resulting in neuronal death and reduction in Aβ clearance. In a healthy individual Tau protein is a microtubule-associated protein. In AD, tau is hyperphosphorylated developing into a neurofibrillary tangle (NFTs). As an NFTs, it accumulates outside neuronal cells and causes neurotoxic activities like Aβ. The function and presence of these two proteins are supposedly the primary cause of AD. The Aβ and Tau AD model explain the decline in neuronal numbers leading to a reduction in memory capacity in AD.

In vivo neurogenesis is unable to be used to increase memory capacity in AD patients. The main reason for this is that neurogenesis decreases with age(9) and AD is commonly seen, in the elderly. Nevertheless, some studies have shown an increase in neurogenesis, in neurological diseases, e.g., Huntington's. Despite this, memory capacity cannot increase because only 0.2% of the damaged neurons are replaced(9). Not enough to restore normal cognitive function. Thus, in vivo neurogenesis is, unlikely to restore memory capacity in AD patients.

Furthermore, several studies state a reduction in neurogenesis in AD. Due to, neuroinflammation and synaptic degeneration (caused by loss of neurons), from Aβ and tau accumulation. Therefore, neurogenesis level in AD is less than 0.2%(9), which is not enough to reverse the long-term neuronal degradation of AD. Hence, neurogenesis is unlikely to increase memory capacity in AD patients.

Unlike in vivo neurogenesis, SCT has a higher likelihood of increasing memory capacity in AD. There are mountains of successful evidence supporting this (26 for adult neural stem cells (NSCs) alone)(6). Animal experimental models were used to stimulate the symptoms of AD in these experiments. Many of which used mouse models. Among these are, Lee et al., 2015(8) studies state that neural stem cells can reduce Aβ levels in 13 months old APP/PS1 mouse and hNSCs modulated NSCs prevented hyperphosphorylation of tau proteins. A possible mechanism in which NSCs reduce Aβ concentration is by increasing neprilysin (NEP)(10) levels. NEP is a peptidase that breaks down Aβ. Plus, the initiation of Aβ phagocytosis(8), by microglial cells. Microglial cells are phagocytes located in the brain. Studies showing a reduction in Aβ levels, via SCT, are numerous within the literature and for other symptoms such as neuroinflammation. Whereas there aren’t many for NSCs and tau interaction(10). More research is required to figure this out. As a result of the above studies, there is high confidence within the scientific community that SCT could treat AD by restoring neuronal levels, increasing memory capacity.

However, the genetic difference between mice and human, bring forth questions about SCT success rate in increasing memory capacity. Mice and humans are genetically different, with only 85%(11) similarity. Hence, the neurological environment between mice and humans might be different based on the biochemical and physiological structure present. An increase in memory capacity using this technique might be something only seen in mice, not humans.

Even so, if stem cell transplantation were to be performed in AD models more genetically similar humans, compared to mice. An increase in memory capacity in AD patients might be ineffective. Due to current AD animal models, isn't an accurate reflection of AD pathophysiology, in humans. Thanks to our lack of understanding of AD development. The current Aβ and tau model has been under scrutiny with new evidence showing, a decrease in these proteins does not lead to improvements in cognitive functions. Plus, current animal AD models utilising this theory are, unable to produce the same pattern of neurodegeneration, as seen in humans. Among these are transgenic mice model (most popular AD model) expressing Aβ or tau, which result in an earlier cognitive impairment onset or a mutated tau. That result in motor deficit not seen in human AD(12). Also, the difference proteins present in non-human primates weakens this AD model similarity to human AD. Since normal AD proteins, like NFT, are uncommon in non-human primates. Only one chimpanzee (98% genetically like humans(13) has developed NFT(12). With all these inaccuracies seen in current AD animal models, the success of SCT increasing AD memory capacity decreases.

However, the inconsistencies in animal AD models, have not prevented the initiation of clinical/preclinical trials, using this technique. There have been clinical trials conducted using this technique, with no success(10). One of the reasons for this is a lack of efficient biomarkers to detect AD during its early stage(10).

Currently, there are no other methods that can increase memory capacity in AD. This is expected, as SCT is the only method able to replace/add body cells. Production of mechanical devices that function as neurons have yet to be developed, in AD research. Mainly due to our lack of understanding of the brain and how tiny neurons can have such a diverse function. Direct interaction between the brain and a machine, is a field requiring more research. Similarly, neural organoids are a possible way of increasing memory capacity in AD suffers. Though much research is required, to see if this is possible. Currently, it is only being considered a technique to study AD development.

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