The cellular memory hypothesis assumes information storage at the molecular genetic and cellular levels. The best-known example of cellular memory is with the antigen memory of the immune system. Meanwhile, the BMI1 protein of cellular memory is associated with carcinogenesis.
What is cellular memory?
The cellular memory hypothesis assumes information storage at the molecular genetic and cellular levels. An adult human has 100 trillion cells, each performing about 100 different tasks. The cellular memory hypothesis states that every single cell in the human body has its own memory. One of the best known mechanisms of cellular memory is in the immune system, which remembers antigens. Cellular memory is not accessible to consciousness and has not yet been conclusively researched. Observations in mammals such as rats seem to support the hypothesis. For example, rats ingested dissolved cocaine for prolonged periods of time and still showed changes in synaptic activity months later characterized by an output of dopamine. This dopamine output in the reward center has been linked to the concept of cellular memory and is thought to be one of the key effects for substance addiction and relapse in treated addicts. Recent studies have demonstrated that individual cells have limited memory even for external heat and current stimuli. The hypothesis of cellular memory has thus been consolidated. For example, trauma and disease are thought to be stored at the cellular level. Alternative medicine methods such as bioresonance attempt to erase and purge such stored information.
Function and task
The cellular memory of the immune system remembers antigens that have been fought in the past. Through this process, it recognizes pathogens more quickly after initial contact and fights them more effectively or strongly. This principle is the basis of the acquired immune response and is supported by vaccination. However, a cellular memory apparently underlies not only the immune system. All body cells are supposed to remember certain events. Certain genes in plants, for example, allow cells to pass on information about their own genetic fate to all daughter cells. This is what the University of Heidelberg has discovered in molecular biology studies on a model plant. There appear to be structural similarities between the responsible proteins of the model plant and the human protein network, suggesting a similar cell memory in humans. The studies took place on a plant with impaired cellular memory functions. Immediately after germination, individual areas of its cotyledons reverted to embryonic structures. Molecular genetic studies proved that the cotyledons corresponded to somatic embryos. Accordingly, the structures were generated by differentiated cells. In plants without cell memory disorders, the daughter cells are informed about the fate of the mother cells. Responsible for this are two different genes whose defect causes the observed disturbances of cellular memory. These genes are responsible for coding two different proteins that resemble the human BMI1 protein. The protein is structurally a part of molecular mechanisms. For example, in plants and humans, the BMI1 protein marks components of the genetic material, also known as histones. This chemical tag turns off the gene at a specific time and can be passed on to daughter cells with unchanged DNA code during cell division. The coding genes for the BMI1 protein thus enable cells to pass on information about their own genetic fate to subsequent cell generations. Also in favor of cellular memory is a study published in 2000 that examined behavioral changes in ten recipients of a heart transplant. All recipients had up to five new behavioral patterns after transplantation, which the researchers demonstrated in the transplant donors and attributed to the transplantation.However, these observations are declared unreliable by contemporary medicine and are associated with the psychological stress situation of the recipients.
Diseases and ailments
For example, cellular memory can cause discomfort in the context of so-called pain memory. Pain-induced arousal undergoes reinforcement and thus outlasts the period during which a pain stimulus actually affects the individual. The excitatory amino acids are particularly relevant for this mechanism, for example glutamate. These neurotransmitters initiate an excitation cascade. During the excitation cascade, the nerve cells emit various messenger substances that are said to influence the transcription factors. This influencing of transcription factors activates the genetic basis of the affected cell. Long-lasting nerve cells thus activate the so-called protooncogenes, which increase the transcription rate at the target genes. In this way, genetic information is converted into structural information at the morphological level. As a result, new ion channels and receptors are formed in the nerve cell. The production of neurotransmitters and neurohormones increases. Proteins are stored in certain areas of the nerve cells, which are considered the basis of cellular pain memory. The pain memory can cause an amplification of pain signals in the long term through the mechanisms described. Thus, long-lasting pain becomes permanently engraved in the receiving neurons. Overrepresentation of the BMI1 protein also appears to play a role in the development of several cancers, including bladder, skin, prostate, breast, and ovarian cancers. Inhibition of the protein is therefore now used in cancer therapy, for example in ovarian cancer and skin cancer that do not respond to measures such as chemotherapy. Inhibition of the protein has been shown to reduce the self-renewal mechanisms of cancer cells. In mice, the reduction of the protein even extinguished the cancer cells in the long term, curing the animals of their cancer.
