Microchimerism may be the cause of psychiatric disorders

微chimerismism是怀孕期间胎儿和母体细胞的双向交换（图1）。怀孕是嵌合体的最常见和自然原因，造血细胞的双向运输是通过胎盘发生的。因此，我们都出生于Microchimera [1,2]。尽管有许多未解决的问题，但人们认为嵌合体在人类健康中具有重要作用。多年来，孕产妇微chimer剂细胞（MMCC）在器官修复和癌症治疗中的临床作用刚刚开始了解。尽管嵌合主义的使命是直接的，但主题是深刻的。Chimerism具有疾病和健康益处的潜力。最近的研究表明，孕妇的压力和妊娠感染会影响胎儿神经发育，并增加胎儿未来生活中神经或精神疾病的风险。本文介绍了MC在精神病病因中的作用。

The relationship between microchimerism and psychiatric disorders

怀孕期间母亲和胎儿之间的双向细胞转移是一种生理现象（图1）。因此，我们都在微观上出生。今天，不确定MC的原因或其任务是什么。因此，MC的生理任务是一个神秘而不完整的问题。MC也被视为免疫系统的生理组成部分。与妊娠有关的迁移祖细胞（FPC）已显示与多个母体器官合并。这些发现支持胎儿细胞经常穿越人类血脑屏障并且大脑中的MC相对普遍的可能性。然而，这些胎儿细胞（FC）与大脑的关联，它们的长期生存和分化尚不完全了解。但是，FPC被证明成熟并分化为母脑中的神经元。在胎儿母亲MC中，表明FPC与母体大脑的各个区域连接在一起，直到7Thmonth after birth and became permanent [3]. In addition to expressing neural stem cell or immature neuron markers, FPCs were expressed mature neuron markers and indicated that they adopted a neuron fate. In addition, neuronal maturation of these cells was observed with increasing axonal dendritic complexity. Thus, FPCs appear to undergo a molecular and morphological maturation program similar to that observed during adult neurogenesis.

生理病理状态

每个生理事件都有生理病理状态。在怀孕的头几个月中，母亲的病毒感染正在破坏生理学。事实上，由于母亲的病毒感染，孕产妇细胞在怀孕的前4.5个月中从母亲传递到胎儿。这样，胎儿就受到了病毒疾病的保护。传染病可以增加母亲和胎儿之间的常规细胞迁移。通过以保护胎儿的母亲的细胞在返回之前在各种组织和器官的构造中起作用。这些MMCC的功能有不同的解释，这些MMCC在胎儿组织中定居并且不返回。众所周知，由于遗传，表观遗传学和环境因素的相互作用，人类的神经发育结果。在哺乳动物中，大脑发育的基础是在出生前完成的。我们认为这些非返回细胞是导致生理病理学MC的原因。 Recent findings suggest that there is a relationship between schizophrenia and immune system disorders. The relationship between maternal infection and neurodevelopmental disorders has long been known. Although schizophrenia was considered a syndrome of different biological backgrounds, the inclusion of immune system disorders may be one of the common mechanisms. The strongest evidence for maternal infection increasing risk for a mental disorder in the offspring is the connection between schizophrenia and maternal respiratory infection [4,5]. An increase in the amount of viral infection and schizophrenia was detected in winter and spring. Thus, the risk for schizophrenia in the offspring was increased 3-fold by infection in the second trimester [4]. Numerous animal studies demonstrate that prenatal or early postnatal infections can result in both acute and persistent neurological and behavioral abnormalities in offspring resembling autistic traits or schizophrenia [4,6]. Modeling this risk factor in animals, when influenza infection is induced in pregnant rodents during pregnancy, their offspring Show several behavioral and histological abnormalities consistent with human mental illness [7]. In 1964, the incidence of schizophrenia in the population exposed to rubella epidemic increased from 1% to 20% [8]. Subsequent studies have shown that historical outbreaks such as influenza, measles, mumps, chicken pox and polio are associated with schizophrenia [9]. However, several prospective studies [10,11] revealed a relationship between maternal viral infection and psychiatric disorders in offspring [12,13]. During the months of winter and spring when the incidence of viral infections as well as the incidence of schizophrenia births are high, supporting our hypothesis [14]. How can the above pathogens provide the risks of psychotic disorder? The common response to these pathogens is maternal immunity. Indeed, exposure to environmental pollutants leading to high immune responses such as maternal autoimmune disorders, allergies, asthma and acute stress has been reported to increase the risk of schizophrenia [10,11]. All this evidence points to the important role of neuro-inflammation and immune system in the pathophysiology of schizophrenia [14]. However, there were numerous reports supporting the hypothesis that immune activation is a risk for the onset of schizophrenia in adulthood [15,16]. Schizophrenic clinical observations observed after bone marrow transplantation will significantly enhance our understanding of the importance of the immune system in schizophrenia [17,18].

但是，我们认为母体细胞可以通过母亲的人类历史向后代迁移而获得的知识。鉴于DNA存储了25亿吨信息的能力，将在整个人类历史上获取的信息转移到新一代不应该很难。因此，胎儿细胞穿过母亲的身体，并有机会向母亲在整个人类历史上获取的信息中学习。之后，这些细胞可能会回到乳房组织，并通过母乳喂养从母亲那里复制的家族信息返回婴儿。这些后代中这些细胞的命运尚未得到充分描述。在最近的一项研究中；已经证实，在后代的血液和大脑中检测到母体细胞，这些细胞分化为脑中的神经元和神经胶质细胞[1]。这向我们表明，由于母乳喂养，大脑中MC的存在。因此，可以保证将获得的恐惧，行为和心理利益转移到新一代。除了胎儿脑发育外，MMCC还会影响产后认知表现和行为。

Evidence from research over the past decade shows that the parental environment can have a profound impact on future generations. This supports our thinking; a recent study showing that parent ‘memory’ was inherited between generations of Drosophilla melanogaster flies [19], it was reported that new behavior continued for five generations, not just one generation. Researchers have shown that even though neuronal coded ancestral behavior is not thought to be hereditary for generations, environmentally triggered modifications that of parental experiences, may allow the memory to remain hereditary. Therefore, it is important to examine the impact of parental experiences affecting future generations. There are many human studies that show that parental stress environments affect at least the next generation. Dutch Hunger Winter [II. Close to the end of World War I, the Dutch famine of 1944-1945] and a generation of food deprivation have shown a number of studies showing that offspring and grandchildren may experience permanent metabolic changes. There were some studies showing that there is an increase in anxiety in children of families with paternal post-traumatic stress disorder. There were also some interesting studies in mice and other model systems. All this generally indicates that there is some extra environmental information that is transferred off-chromosomally to children. However, Drosophila melanogaster flies can have highly conserved molecular mechanisms despite human and all animal species, and many things can work similarly.

最近的研究表明，响应产前应激的大脑发育可能会因遗传倾向而与遗传易感性无关。观察性研究还表明，产前不良的环境影响（例如母体压力和感染）会影响胎儿神经发展，并增加未来生活中神经或精神疾病的风险[20-22]。神经发育途径的破坏会影响认知和精神障碍，并影响未来的大脑功能，并可能增加后来生活中神经发育和精神疾病的风险[23]。胎儿的适应过程对诸如母性应激和/或母体感染等负有压力非常敏感。在这种情况下，慢性应激状况会影响孕妇[24]。此外，这种不良生活事件可能会对怀孕期间的孕产妇健康构成重大威胁。母亲在怀孕期间经历的过度压力会导致自闭症谱系障碍[25]，抑郁症状[26,27]，焦虑症，人格障碍，饮食失调[28]和注意力不足/多动障碍[21,29,30]。除了高水平的压力感知外，怀孕期间的孕产妇感染还可能干扰胎儿的神经发育，并可能增加后代神经功能障碍，精神疾病和自闭症谱系障碍的风险[31]。

Too many maternal cells for to fight infectious diseases that pass to the fetus cannot return to the mother’s body. These cells are maternal leukocytes and lymphocytes somatic cell nature. When suitable agents were used, these cells are “dedifferentiated” and can be transformed into stem cells. Fetal cell medium is a medium where stem cells are dense. We believe that maternal cells passing into fetus are first differentiated into stem cells by dedifferentiating, then differentiated (Redifferentiated) and involved in the construction of tissues and organs. This will cause allo-immunity because the DNAs of the cells involved in the construction of tissue organs are different. Today, we must recognize that maternal microchimeric cells cause autoimmune diseases, and that these cells are the etiologic cause of alloimmune diseases, and should be treated accordingly (also in psychiatric diseases). If the maternal cells that acquire physiopathological features participate in the production of the brain, there are 2 different groups of DNA in the brain. In this case, two different neuromediator-receptor groups will be present in the same brain tissue. The production of each DNA is individual. Chaos physics rules begin to work and the brain’s architecture (configuration) changes as the initial conditions change. In babies born with brain changing architecture, ‘Soft Neurological Symptoms’ were detected [32].

第一次攻击后，胎儿母细胞迁移的概念可以解释1/3精神分裂症患者的完全恢复吗？

If these nomadic cells are unable to produce stem cells that can sustain them, schizophrenia will heal after the first episode, since new nomadic cells that are cleared from the schizophrenic brain are not replaced. If the nomadic cells were able to produce stem cells that would allow them to survive, they would produce new nomadic cells instead of being dragged into apoptosis and destroyed. In this case, schizophrenia would have gained chronicity.

FETö-Fertnal细胞迁移可以解释“幻觉”的概念。换句话说，如果脑组织中有两个不同的DNA，则神经分解剂受体的产生将被个性化。即使精神分裂症脑细胞产生的多巴胺达到游牧细胞库，它也无法结合，因为“再分配频率”不同。因此，由于多巴胺饥饿，游牧细胞受体将继续要求多巴胺，多巴胺将不断产生和传递。因此，环境中会有相对丰富的多巴胺。在这种情况下，多巴胺将到达并激活听力受体，而精神分裂症的人会听到声音。振动频率在一项关于果蝇黑色素果蝇苍蝇的研究中，该室的隔室始终找到了苹果本质的烟道。但是，当在苹果精华中使用氘或trip而不是氢时，果蝇无法正确找到苹果本质的区域。因为将剂量或trium添加到苹果本质中，所以它改变了本质的振动频率，因为这些物质比氢更重。我们可以将振动频率与驱动我们汽车的射频开关进行比较。 In appearance, although all keys and slots are similar, one key cannot start another car because the radiofrequency is different. The resonance frequencies of the neuromodulatory receptor pair produced by each DNA are also different. We think that psychotic behavior seen in this postpartum mother may be seen in this way. In a recent study, we reported that there was significant difference between women with postnatal depression and healthy women. MMc prevalence was significantly greater in women with postnatal depression than control groups [32]. Mc is known to play an etiological role in autoimmune diseases, and may also be the causative factor in the development of schizophrenia and postpartum psychosis [33].

We believe that Mc may be an important alternative explanation to the etiology of psychiatric diseases. Thus, numerous studies demonstrate that prenatal or early postnatal infections can result in both acute and persistent neurological and behavioral abnormalities in offspring resembling autistic traits or schizophrenia. Current studies will provide valuable insights into the effects of the immune system on brain and behavior, and represent an important potential step towards more personalized medicine for patients with schizophrenia.

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