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Alzheimer’s disease (AD) is a neurological disorder that involves plaque accumulation and neurofibrillary tau tangles which contribute to degradation of the nerve cells. AD is characterized by decreasing cognitive function, memory impairment, and neuronal loss. There are complications with detecting and diagnosing AD in its early stages and because of this, studies focus on characteristics of lesions in AD brains.
The first AD lesion discovered in human brain tissue shows amyloid plaques consisting of Aβ peptide aggregation in insoluble fibrils. Neurofibrillary tangles are found in the brain cells that are made of insoluble intertwined tau fibers. The most common Aβ is Aβ1-42/Aβ1-40, which is most prone to toxic conformational changes causing nerve death and amyloid plaque formation. The increase of the amyloid ratio of (Aβ1-42) longer amyloid-β to (Aβ1-40) shorter amyloid-β advances the development of AD. The mutation phenotype shows an increased production of high fibrillogenic Aβ1-42 peptides along with amyloid precursor protein (APP). Neurotoxic Aβ deposits, modified by metal-binding, play a crucial role in Alzheimer’s disease pathogenesis involving its ability of synaptic dysfunction and cognitive loss in the brain when accumulated. Aβ accumulation is the proteolytic product of amyloid precursor protein (APP). APP is a single-pass transmembrane protein in nerve cells. Aβ accumulation occurs via multiple pathways that can be affected by certain factors. Amyloid deposits are identified by the Aβ positron-emission tomography (PET) imaging or measurement of the amyloid-beta in the cerebral fluid. Many questions arise about finding treatments for this neurodegenerative disorder, it still remains unclear of what can stop the increased accumulation of Aβ peptide in neural synapses of a human brain with AD. Studies have shown productive effects of Aβ-induced neuronal cell death and Aβ accumulation from nicotine, however, it is not the only treatment with a productive role against the pathogenesis of AD. A food supplement involving digested black sesame pigment exhibits abilities of marked antioxidants and heavy metal binding properties These two different treatments and their separate effects against Aβ accumulation in the neural synapses are expressed throughout this paper.
Neuronal activity in the brain plays a role in the production and release of the Aβ peptide which leads to Aβ plaque accumulation. Plaque deposits are formed when Aβ accumulates in the synapses. Aβ usually accumulates in parts of the associate cortex that present high structural and functionally connectivity. Not all areas are subjected to accumulation, suggesting that neuronal activity is not alone in the role of regional vulnerability. Brain nodes can be vulnerable to amyloid accumulation due to the spreading of amyloid through the synaptically connected areas with elevated concentration of synapses. The synaptic terminals are the principal sites of beta-amyloid peptide release that gradually accumulates in extracellular space of the downstream regions. Neurodegenerative diseases progress from the mechanism of disease-associated misfolded protein passage that goes from neuron to neuron.
Current studies have shown that Aβ deposits at different levels can be identified using certain methods. Amyloid deposits can be identified by measurement of the cerebral spinal fluid or the (PET) imaging, as stated previously. This is where blood-base amyloid biomarkers come into place that are involved in the cerebral spinal fluid. These plasma biomarkers have been able to detect different levels of Aβ deposits within individuals. The biomarkers were developed by using immunoprecipitation-mass spectrometry (IP-MS). The Aβ precursor protein (APP) and their composites are able to predict individual brain amyloid-beta-positive or -negative status. The plasma Aβ composite biomarker’s and the CSF Aβ biomarker’s performance were highly comparable to each other. Data has shown that the different types of the Aβ related biomarkers, (plasma, CSF, PET-imaging), show correlation indicating plasma Aβ biomarkers are strongly linked with CNS status of Aβ deposits.
Although the plasma biomarkers still have some issues that need to be addressed, preventative agents to AD have been discovered.
One substance that shows productive effects as a treatment toward the inhibition of Aβ accumulation is nicotine, the major component of cigarette smoke extracts. It is a significant risk factor for AD that is associated with Aβ plaques. Nicotine has beneficiary factors such as reduction of memory impairment in aging, chronic stress, hypothyroidism, and brain lesions. Nicotine causes autonomic ganglia and nerve terminals to release neurotransmitters norepinephrine, ACh, NO, and polypeptides. Nicotine is a modulator of α7 nicotine acetylcholine receptors (α7nAChRs) that mediate these effects. Nicotine shows potential of targeting the pathology of AD because of its anti-inflammatory, pro-cognitive, and anti-protein aggregation effects. The α7nAChRs expressed in the brain, are involved in cognitive function and interact with Aβ. Studies have shown that nicotine increases the extracellular Aβ1-40 from wildtype APP and mutant APP.
The culture media from London and Sweden show an increase in these Aβ1-40 peptides although neither show any effect in the Aβ1-42 peptides. This was caused by an increase in the β-secretase (BACE1) which cleaves APP to release soluble APP fragments prior to Aβ production. Phosphorylation of APP regulates amyloidogenic processing by BACE1. It was also shown that nicotine can increase the shorter amyloid, Aβ1-40 monomers, to reduce the Aβ1-42/ Aβ1-40 amyloid ratio expressing APP. This protects against the Aβ1-42 induced fibrillogenesis. Pathways involved in nicotine-mediated protection against Aβ toxicity were identified. The signaling pathway that was analyzed was the alpha7-nAchR/phosphatidylinositol-3-kinase (PI3K). Nicotine demonstrated neuroprotective effects against Aβ-oligomer-induced damage in both of the pre and postsynaptic regions of an AD brain. However, consuming high doses of nicotine can be quite toxic and even lethal. Studies show that the disorder of AD is twice as low in smokers than in age-matched controls. Since there are risk factors involved with nicotine, alternative treatments were examined.
Another substance that shows positive effects on the treatment of Aβ plaque accumulation is digested BSP, material from plant origin. Black sesame pigment (BSP) is a preventive agent that exhibits antioxidant and heavy metal binding properties with a potential to be a food supplement. Exposure to heavy binding materials that are toxic cause impairment of the central nervous system which results in cognitive abnormalities. The bioaccessible fraction of BSP stimulated gastrointestinal digestion against key enzymes involved in Alzheimer’s disease. Binding experiments were conducted to determine the relationship between the amount of metal binding at different doses of BSP. BSP activity is at its maximum in the intestinal environment. While in the presence of the bioaccessible fraction of BSP, there was 80% inhibition of the acetylcholinesterase-induced aggregation of the Aβ 1-40, as well as inhibition from self-induced Aβ 1-42 aggregation and beta-secretase (BACE-1) activity. Aβ starts its accumulation with increased deposits of amyloid by the processing of the APP by BACE-1. With the inhibition that BSP produces, it can act as a preventative factor for Aβ deposits. BSP transformations occur due to moderate alkaline hydrolytic reactions under certain pH environments that mimic the intestinal environment. It was found that AChE can bind to amyloid-beta and accelerate its aggregation through peripheral anionic sites (PAS). Inhibitors designed to reach PAS and catalytic anionic site of AChE simultaneously are the source of multitarget anti-Alzheimer compounds. Sesame ligands, such as sesaminol and sesamol, have shown efficient inhibition of the AChE and the Aβ oligomerization and fibril formation.
The use of BSP as a food supplement or functional food provides a new perspective on the prevention of Alzheimer’s disease. The development of multi-target anti-Alzheimer treatments has been designed to target Aβ formation and aggregation and AChE activity. These properties of the black sesame pigment and the multitarget anti-Alzheimer treatments can open new opportunities for preventative actions of Alzheimer disease. On the other hand, using black sesame pigment as an ingredient in functional food could cause allergic reactions in some users. It is still a foreign component to the human bodies and not every patient would react in the same ways.
Neuronal activity plays the main role in amyloid accumulation in the synapses of the AD brains. Amyloid accumulation is expressed as a ratio of large amyloids to small amyloids, Aβ 1-42/ Aβ1-40. Two substances were discussed as preventative treatments, the Black Sesame Pigment (BSP), and nicotine extracted from cigarette smoke. BSP showed inhibition of the small amyloids Aβ1-40 as well as inhibition of large amyloids Aβ1-42. This productive effect decreases the amyloid accumulation ratio in AD. Nicotine extracted from cigarette smoke showed a decrease in the small amyloid Aβ1-40 levels, which decreases the overall amyloid ratio Aβ1-42/ Aβ1-40. This shows an alternative way to the approach of decreasing Aβ accumulation in AD.
I believe that when comparing nicotine to BSP in respect to preventatives for AD, BSP shows a more useful and easily accessible opportunity as a protective measure. The black sesame pigment is a low-cost attainable resource from plant origin that is a healthier choice in contrast to nicotine. Both treatments act as preventative agents for AD, but nicotine is an addictive agent involved in smoking production whereas BSP can be used as a food supplement or component in functional food. Nicotine did not affect all of the components that contribute to neurotoxicity in AD. Therefore, the involvement of nicotine extract from cigarette smoke does not show a competitive treatment compared to the major consequences that smoking produces. The black sesame pigment (BSP) not only showed inhibition of 80% of the acetylcholinesterase-induced Aβ1-40 aggregation but also showed inhibition of self-induced Aβ1-42 aggregation and β-secretase activity. I believe that BSP is a better alternative than nicotine in the prevention of Aβ accumulation of AD. The ultimate goal of both of these treatments is to contribute productive and protective effects against the accumulation of Aβ in AD. Although BSP has not been released to patients and allergic reactions have not been tested, it presents itself as a better choice for treatments towards the fight against AD. In the future, I believe there will be experiments involved with patients of AD and the usage of food supplements containing BSP. The properties of BSP and nicotine give researchers new perspectives on how to treat amyloid accumulation. I believe that further investigation of these two treatments is needed before official use within the public.
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