黑色素,一种无处不在的深色颜料,在免疫系统中起着重要的作用,包括清除响应紫外线辐射吸收而形成的活性氧,吸收金属,热调节,药物摄取,先天免疫系统功能,氧化还原,和能量转导。许多组织类型,包括大脑,心,动脉,卵巢,和其他人,含有黑色素。几乎所有细胞都含有黑色素的前体。越来越多的黑色素和/或神经黑色素丢失的疾病被认为具有感染性病因,例如,阿尔茨海默病(AD),帕金森病(PD),路易体痴呆(LBD),和白癜风。AD,PD,LBD,白癜风与疱疹病毒有关,进入黑色素体并导致细胞凋亡,肠道菌群失调和炎症。疱疹病毒也与肠道菌群失调和炎症有关。我们推测在正常的健康状态下,黑色素保留了它从电磁辐射中吸收的一些能量,然后用于燃料电池,来自ATP的能量被用来补充能量供应。我们进一步推测黑色素的丢失会减少细胞的能量供应,在AD的情况下,PD,和LBD导致无法维持免疫系统防御和去除与疾病相关的斑块,这似乎是免疫系统试图根除这些神经退行性疾病中的病原体的一部分。此外,试图解释为什么去除这些斑块不会导致认知和情绪的改善,以及为什么这些个体的认知和情绪起伏不定,我们假设不是斑块引起认知症状,而是,更确切地说,免疫系统对病原体的反应导致的大脑炎症。我们的理论认为,黑色素中保留的能量与ATP成反比关系的细胞得到了研究的支持,这些研究表明,在黑素瘤中,ATP产生的变化与黑色素水平有关。白癜风,健康的细胞因此,黑色素水平的改变可能是许多疾病的核心。我们建议调节黑色素水平可能为治疗发展提供新的途径。
Melanin, a ubiquitous dark pigment, plays important roles in the immune system, including scavenging reactive oxygen species formed in response to ultraviolet radiation absorption, absorbing metals, thermal regulation, drug uptake, innate immune system functions, redox, and energy transduction. Many tissue types, including brain, heart, arteries, ovaries, and others, contain melanin. Almost all cells contain precursors to melanin. A growing number of diseases in which there is a loss of melanin and/or neuromelanin are increasingly thought to have infectious etiologies, for example, Alzheimer\'s disease (AD), Parkinson\'s disease (PD), Lewy Body Dementia (LBD), and vitiligo. AD, PD, LBD, and vitiligo have been linked with herpesvirus, which enters melanosomes and causes apoptosis, and with gut dysbiosis and inflammation. Herpesvirus is also linked with gut dysbiosis and inflammation. We theorize that under normal healthy states, melanin retains some of the energy it absorbs from electromagnetic radiation, which is then used to fuel cells, and energy from ATP is used to compliment that energy supply. We further theorize that loss of melanin reduces the energy supply of cells, which in the case of AD, PD, and LBD results in an inability to sustain immune system defenses and remove the plaques associated with the disease, which appear to be part of the immune system\'s attempt to eradicate the pathogens seen in these neurodegenerative diseases. In addition, in an attempt to explain why removing these plaques does not result in improvements in cognition and mood and why cognitions and moods in these individuals have ebbs and flows, we postulate that it is not the plaques that cause the cognitive symptoms but, rather, inflammation in the brain resulting from the immune system\'s response to pathogens. Our theory that energy retained in melanin fuels cells in an inverse relationship with ATP is supported by studies showing alterations in ATP production in relationship to melanin levels in melanomas, vitiligo, and healthy cells. Therefore, alteration of melanin levels may be at the core of many diseases. We propose regulating melanin levels may offer new avenues for treatment development.