Table of contentsIntroductionAmyloid accumulationAβ identificationEffect of nicotine on the accumulation of AβPreventive digestive BSP for the accumulation of AβConclusionExpert opinionIntroductionThe disease Alzheimer's disease (AD) is a neurological disorder that involves accumulation of plaques and neurofibrillary tangles of tau that contribute to the breakdown of nerve cells. AD is characterized by decreased cognitive functions, memory impairment and neuronal loss. There are complications associated with the detection and diagnosis of Alzheimer's disease in its early stages and for this reason studies focus on the characteristics of lesions in Alzheimer's disease brains. Say no to plagiarism. Get a tailor-made essay on “Why violent video games should not be banned”?Get the original essayFirst AD lesion discovered in human brain tissue shows amyloid plaques made of aggregation of Aβ peptides in insoluble fibrils . Neurofibrillary tangles are found in brain cells 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. Increasing the amyloid ratio from (Aβ1-42) longer amyloid-β to (Aβ1-40) shorter amyloid-β advances the development of AD. The mutation phenotype shows increased production of highly fibrillogenic Aβ1-42 peptides as well as amyloid precursor protein (APP). Neurotoxic Aβ deposits, modified by metal binding, play a crucial role in the pathogenesis of Alzheimer's disease, implicating its ability to cause synaptic dysfunction and cognitive loss in the brain when they accumulate. The accumulation of Aβ is the proteolytic product of amyloid precursor protein (APP). APP is a single-pass transmembrane protein in nerve cells. Aβ accumulation occurs via several pathways that can be affected by certain factors. Amyloid deposits are identified by Aβ positron emission tomography (PET) imaging or by measuring amyloid beta in brain fluid. Many questions arise regarding the search for treatments for this neurodegenerative disease, but it remains unclear exactly what can stop the increased accumulation of Aβ peptide in the neural synapses of a human brain with AD. Studies have shown the productive effects of Aβ-induced neuronal cell death and Aβ accumulation from nicotine. However, it is not the only treatment playing a productive role against AD pathogenesis. A dietary supplement containing digested black sesame pigment exhibits marked antioxidant and heavy metal binding capabilities. These two different treatments and their distinct effects against Aβ accumulation in neural synapses are expressed throughout this article. Amyloid accumulation Neuronal activity in the brain plays a role in the production and release of the Aβ peptide which leads to the accumulation of Aβ plaque. Plaque deposits form when Aβ accumulates at synapses. Aβ typically accumulates in parts of the associated cortex that have high structural and functional connectivity. Not all areas are subject to accumulation, which suggests that neuronal activity is not the only one to play a role in regional vulnerability. Brain ganglia may be vulnerable to amyloid accumulation due to the spread of amyloid across areas synaptically connected witha 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 mechanism of misfolded protein passage from one neuron to another. 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 measurement of cerebrospinal fluid or by imaging (PET), as previously discussed. This is where blood amyloid biomarkers involved in cerebrospinal fluid come into play. These plasma biomarkers were able to detect different levels of Aβ deposits in individuals. The biomarkers were developed using immunoprecipitation mass spectrometry (IP-MS). Aβ precursor protein (APP) and their composites are capable of predicting the beta-positive or negative amyloid status of the individual brain. The performance of the composite plasma Aβ biomarker and the CSF Aβ biomarker was highly comparable. Data showed that different types of Aβ-related biomarkers (plasma, CSF, PET imaging) show a correlation indicating that plasma Aβ biomarkers are strongly related to the status of Aβ deposits in the CNS. Although plasma biomarkers still have some problems that need to be resolved. be addressed, preventive agents against AD have been discovered. Effect of Nicotine on Aβ Accumulation One substance that exhibits productive effects as a treatment for the inhibition of Aβ accumulation is nicotine, the major component of cigarette smoke extracts. It is an important risk factor for AD associated with Aβ plaques. Nicotine has beneficial factors such as reducing memory problems related to aging, chronic stress, hypothyroidism and brain damage. Nicotine causes autonomic ganglia and nerve endings to release neurotransmitters norepinephrine, ACh, NO, and polypeptides. Nicotine is a modulator of α7 nicotine acetylcholine receptors (α7nAChRs) that mediate these effects. Nicotine shows the 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 in both wild-type and mutant APP. Culture media from London and Sweden showed an increase in these Aβ1-40 peptides although neither showed an effect on Aβ1-42 peptides. This was due to an increase in β-secretase (BACE1) which cleaves APP to release soluble APP fragments before Aβ production. Phosphorylation of APP regulates amyloidogenic processing by BACE1. It has also been shown that nicotine can increase the shorter amyloid, Aβ1-40 monomers, to reduce the APP-expressing Aβ1-42/Aβ1-40 amyloid 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 demonstrated neuroprotective effects against Aβ oligomer-induced damage in pre- and postsynaptic regions of AD brain. However, consuming large doses of nicotine can be very toxic and even fatal. Studies show that AD is twice as low in smokers as in age-matched controls. Since there are risk factors involved with.