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Protein deposition due to the process of accumulation inside or outside cells causes many neurological diseases such as Alzheimerchr('39')s, Huntingtonchr('39')s or Parkinsonchr('39')s seizures. Parkinsonchr('39')s disease is the second most common neurological disease after Alzheimerchr('39')s, in which patients develop disorders due to the accumulation of leprosy and the destruction of dopamine neurons. Alpha-synuclein protein contains 140 amino acids, the main protein known in lewy body accumulations. During the aggregation process, alpha-synuclein protein monomers bind together as oligomers and eventually become amyloid filaments. So far, there is no drug to stop or delay the progression of Parkinsonchr('39')s, but studies on the molecular mechanism of amyloid formation and the identification of inhibitors are increasing. For this purpose, in this study, the effect of BRICHOS domain resulting from BRI2, which can have various functions, including antimicrobial properties, on the process of alpha-synuclein accumulation as a model protein was investigated.The gene was first optimized and synthesized and then multiplied by PCR. The product was digested by enzymes Xho I and Nde1 and entered the expression vector pET28 a, which was transformed into E. coli bacteria.Finally, the peptide was purified by nickel chromatography. The alpha-synuclein gene was also expressed separately and purified.The anti-cumulative effect of BRICHOS domain on alpha-synuclein fibrillation was investigated using Toflavin T fluorescence method and TEM technique.

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Neurodegenerative disorders are characterized by the progressive deterioration of the central nervous system (CNS).  Depending on the affected regions, patients may experience a broad spectrum of neurological deficits, such as sensory, motor, cognitive, and psychological symptoms. Notably, cholesterol synthesis in CNS occurs in a de novo manner and is distinct from systemic lipid metabolism. However, lipids constitute a large portion of the brain and are involved in crucial brain functions like neurotransmission and synaptic plasticity. Emerging evidence suggests that alterations in lipid metabolism may contribute to the development and progression of different aspects of neurodegeneration, such as neuroinflammation, oxidative stress, and impaired neuronal membrane function.
There are several critical changes in various lipid fractions, like cholesterol and triglycerides (TG), in individuals with neurodegenerative disorders. This narrative review aims to summarize the current understanding of the relationship between lipid profiles and neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). The findings may have important implications for the development of novel diagnostic and therapeutic strategies targeting lipid-related pathways in the management of these debilitating neurological conditions.