IndexIntroductionAmyloid AccumulationAβ IdentificationEffect of Nicotine on Aβ AccumulationDigestive BSP Preventive for Aβ AccumulationConclusionExpert OpinionIntroductionAlzheimer's Disease (AD) is a disorder neurological which involves the accumulation of plaques and neurofibrillary tau tangles that contribute to the degradation of nerve cells. AD is characterized by decreased cognitive function, memory impairment, and neuronal loss. There are complications in detecting and diagnosing AD in its early stages, and for this reason, studies focus on the characteristics of lesions in the AD brain. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essayThe first AD lesion discovered in human brain tissue shows amyloid plaques made up of aggregation of Aβ peptides into insoluble fibrils. Neurofibrillary tangles are found in brain cells made up of insoluble intertwined tau fibers. The most common Aβ is Aβ1-42/Aβ1-40, which is more prone to toxic conformational changes that cause nerve death and the formation of amyloid plaques. Increasing the amyloid ratio between the longer amyloid-β (Aβ1-42) and the shorter amyloid-β (Aβ1-40) advances the development of AD. The mutation phenotype shows increased production of highly fibrillogenic Aβ1-42 peptides together with amyloid precursor protein (APP). Neurotoxic Aβ deposits, modified by metal binding, play a crucial role in the pathogenesis of Alzheimer's disease, involving its capacity for synaptic dysfunction and cognitive loss in the brain when accumulated. Accumulation of Aβ is the proteolytic product of amyloid precursor protein (APP). APP is a single-pass transmembrane protein in nerve cells. The accumulation of Aβ occurs through multiple pathways that can be influenced by certain factors. Amyloid deposits are identified by Aβ positron emission tomography (PET) or measurement of amyloid-beta in brain fluid. Many questions arise about finding treatments for this neurodegenerative disease, but it is not yet clear what can stop the increased accumulation of Aβ peptide in the neural synapses of a human brain affected by AD. Studies have demonstrated productive effects on Aβ-induced neuronal cell death and Aβ accumulation by nicotine, however, it is not the only treatment with a productive role against AD pathogenesis. A dietary supplement involving digested black sesame pigment exhibits marked antioxidant capacity and heavy metal binding properties. These two different treatments and their separate effects against Aβ accumulation in neural synapses are expressed in this article. Amyloid AccumulationNeuronal activity in the brain plays a role in the production and release of Aβ peptide which leads to the accumulation of Aβ plaques. Plaque deposits form when Aβ accumulates in synapses. Aβ usually accumulates in parts of the associated cortex that exhibit high structural and functional connectivity. Not all areas are subject to accumulation, suggesting that neuronal activity is not alone in the role of regional vulnerability. Brain nodes may be vulnerable to amyloid accumulation due to the spread of amyloid through synaptically connected areas with high concentration of synapses. Synaptic terminals are the main sites of release of beta-amyloid peptide which gradually accumulates in the extracellular space of downstream regions. Neurodegenerative diseases progress from the disease-associated misfolded protein passage mechanism thatit goes from neuron to neuron. Identification of Aβ Current studies have shown that Aβ deposits at different levels can be identified using certain methods. Amyloid deposits can be identified by measuring cerebrospinal fluid or (PET) imaging, as stated previously. This is where amyloid biomarkers in the blood that are involved in the cerebrospinal fluid come into play. These plasma biomarkers were able to detect different levels of Aβ deposits in individuals. Biomarkers were developed using immunoprecipitation mass spectrometry (IP-MS). The Aβ precursor protein (APP) and its compounds can predict the positive or negative status of individual brain amyloid beta. The performance of the composite Aβ biomarker in plasma and the Aβ biomarker in cerebrospinal fluid was highly comparable to each other. The data demonstrated that different types of related Aβ biomarkers (plasma, cerebrospinal fluid, PET imaging), show a correlation indicating that plasma Aβ biomarkers are strongly linked to the state of Aβ deposits in the central nervous system. Although plasma biomarkers still present some issues that need to be analyzed and addressed, preventive agents of AD have been discovered. Effect of Nicotine on Aβ Accumulation One substance that shows productive effects as a treatment towards the inhibition of Aβ accumulation is nicotine, the main component of cigarette smoke extracts. It is a significant risk factor for AD associated with Aβ plaques. Nicotine has beneficial factors such as reducing memory impairments in aging, chronic stress, hypothyroidism and brain injury. Nicotine causes autonomic ganglia and nerve endings to release the neurotransmitters norepinephrine, ACh, NO, and polypeptides. Nicotine is a modulator of α7 nicotine acetylcholine receptors (α7nAChRs) that mediate these effects. Nicotine shows potential to target AD pathology due to its anti-inflammatory, pro-cognitive, and anti-protein aggregation effects. α7nAChRs expressed in the brain are involved in cognitive function and interact with Aβ. Studies have shown that nicotine increases extracellular Aβ1-40 of wild-type APP and mutant APP. London and Swedish culture media show an increase in these Aβ1-40 peptides although neither shows any effect on Aβ1-42 peptides. This was caused by an increase in β-secretase (BACE1) which cleaves APP to release soluble APP fragments prior to Aβ production. APP phosphorylation regulates amyloidogenic processing by BACE1. It has also been shown that nicotine can increase the shorter amyloid monomers, Aβ1-40, to reduce the APP-expressing amyloid Aβ1-42/Aβ1-40 ratio. This protects against Aβ1-42-induced fibrillogenesis. Pathways involved in nicotine-mediated protection against Aβ toxicity have been identified. The signaling pathway analyzed was alpha7-nAchR/phosphatidylinositol-3-kinase (PI3K). Nicotine has demonstrated neuroprotective effects against Aβ oligomer-induced damage in both pre- and postsynaptic regions of an AD brain. However, consuming high doses of nicotine can be quite toxic and even lethal. Studies show that AD is two times lower in smokers than in age-matched controls. Since nicotine presents risk factors, alternative treatments have been examined. Preventive digestive BSP for Aβ accumulation Another substance that shows positive effects on the treatment of Aβ plaque accumulation is digested BSP, a material of plant origin. Black sesame pigment (BSP) is a preventative agent that exhibits antioxidant and binding properties.