ROOT CAUSE CURE AND PREVENTATIVE MEASURE FOR SCHIZOPHRENIA AND OTHER MENTAL ILLNESS

Abstract

A method and system for treating schizophrenia and other forms of mental illness, including: given a brain comprising neurons coupled by an axon including an inner core and an outer myelin sheath, and given one or more defects in the outer myelin sheath, repairing the one or more defects in the outer myelin sheath with one or more of a protein and a lipid such that the outer myelin sheath has a substantially constant electrical impedance for the transmission of data energy between the neurons and such that data energy is not undesirably reflected from the direction of a receiving neuron in the direction of a transmitting neuron within the axon.

Claims

1. A method for treating schizophrenia and other forms of mental illness by assessing and modifying a condition of axons of neurons of a brain, comprising: given a brain comprising neurons coupled by an axon comprising an inner core and an outer myelin sheath, and given one or more defects in the outer myelin sheath that interfere with a substantially constant electrical impedance of the outer myelin sheath, first measuring the electrical impedance of the outer myelin sheath to detect and locate the one or more defects in the outer myelin sheath, subsequently repairing the detected and located one or more defects in the outer myelin sheath with one or more of a protein and a lipid such that the outer myelin sheath regains the substantially constant electrical impedance for the transmission of data energy between the neurons, and subsequently measuring the electrical impedance of the outer myelin sheath to confirm the regained substantially constant electrical impedance for the transmission of the data energy between the neurons, wherein the first measuring and the subsequent measuring comprise determining electrical structural return loss (SRL) of the axon and comparing the SRL to a predetermined value.

2. The method of claim 1, wherein the one or more defects in the outer myelin sheath are repaired with one or more of the protein and the lipid such that data energy is not undesirably reflected from the direction of a receiving neuron in the direction of a transmitting neuron within the axon, thereby negating interference with the substantially constant electrical impedance of the outer myelin sheath.

3. The method of claim 1, wherein the one or more defects in the outer myelin sheath are repaired with one or more of the protein and the lipid such that data energy is not undesirably reflected from the direction of a receiving neuron in the direction of a transmitting neuron within the axon, thereby negating interference with the substantially constant electrical impedance of the outer myelin sheath, and thereby not causing the transmitting neuron to receive a reflected data packet energy having the address of the receiving neuron before expecting a reply from the receiving neuron from the connecting axon myelin defect location and then retransmitting the data packet on to the other mesh network neurons which retransmit and spread the receiving neuron addressed data packet over the entire brain until it arrives back at the receiving neuron much later again and again.

4. The method of claim 1, wherein the first measuring comprises first determining and confirming that one or more of a neuregulin level and a gene are abnormal in the brain.

5. The method of claim 4, further comprising repairing the one or more defects in the outer myelin sheath with one or more of the protein and the lipid by controlling neuregulin level accomplishing myelination of the axon.

6. The method of claim 4, further comprising repairing the one or more defects in the outer myelin sheath with one or more of the protein and the lipid via one of gene splicing and gene repair resulting in the myelination of the axon.

Description

BRIEF DESCRIPTION OF THE DRAWINGS

[0028] The present invention is illustrated and described herein with reference to the various drawings, in which like reference numbers are used to denote like system components/method steps, as appropriate, and in which:

[0029] FIG. 1 is a schematic diagram showing a communication system between a pair of brain neurons' signaling through a damaged axon myelination sheath indicating the root cause of schizophrenia and other mental illness and how that root cause can be corrected by the system and method according to an embodiment of the present invention; and

[0030] FIG. 2 is a schematic diagram showing a simple mesh network system built with multiple neurons, their axon multiple ends and the synapses connecting to multiple other neurons indicating how the “Data packet impulses” are fanned out into the eight billion plus neuron brain network.

DETAILED DESCRIPTION OF THE INVENTION

[0031] It is known in the medical research community that myelination of axons enables data packet “impulses” to travel from one cerebral hemisphere to the other via an axon highway called the Corpus Callosum typically in 30 milliseconds. This is compared to 150 to 300 milliseconds through “non-myelinated” axons. In some of the axons, the chemical action potential (Action Potential or impulse) travels at a rate of 1.2 to 250 miles per hour. Also, it is known that mental functions will perform faster with fully and correctly myelinated axons. The means of measuring the “Action Potential or impulse” speed along the approximately one (1) meter long axons of the human spine may be done with microelectrode arrays that have hundreds of electrodes per inch which can induce an “Action Potential signal” into an axon and also receive the “Action Potential signal” from an axon. Mental function speed may be registered by non-invasive technologies such as Electroencephalogram (EEG) and by invasive technologies such as Intracranial electroencephalography (iEEG). The myelination substance is manufactured in sheets by glial cells. An octopus-shaped glial cell called an oligodendrocyte does the wrapping somewhat like electrical tape up to 150 times between every segmented node of the axon. The segmented points between nodes of the myelination allow data repeating for maintaining the signal strength. Biologist, Klaus-Armin Nave of the Max Planck Institute for Experimental Medicine in Gottingen, Germany, discovered that Schwann cells detect a protein called neuregulin that determines whether the Schwann cell wraps more or fewer sheets of myelin around the axon for the optimum thickness of the myelin insulation. It was also found that people who suffer bipolar dis-order and/or schizophrenia have a defect in the gene that regulates production of the protein, neuregulin. The medical research community have amassed all of the pertinent data for the neuron/axon myelination optimization, however, the root cause for disruptive data packet impulses of schizophrenia have eluded them, not because of inadequate brilliance, but merely because their training did not include electrical engineering (physics) communication transmission theory.

[0032] The characteristics and purposes of the myelinated axons and the characteristics of coaxial cables are undeniably the same. The medical research community's peer reviewed papers refer to the data packet energy passed from one neuron to another as “impulse”. We will also refer to the data packet energy as “data packet impulses”.

[0033] It is also known in the medical research community that without myelin, the data packet impulse (in their terms) “leaks and dissipates”. They have found that maximum conduction velocity requires strict proportional myelination insulation to the diameter of the bare axon fiber. The ratio of bare axon diameter divided by the total fiber diameter (including the myelin) is 0.6 for optimum data packet impulse speed along the axons.

[0034] The electrical data packet impulse travel through axons are bound by physical laws, physics and chemistry, thus, follow the same limitations of electronic coaxial cables that have defects concerning the change of impedance along the transmission route of the data packet energy. As it is seen in the following electrical engineering description of coaxial cable data packet impulse “reflection”, the same physics and chemistry can be applied to damaged, imperfectly applied, or genetically missed myelination of axons. Where the referenced frequency of the coaxial cable is noted, the frequencies of the data packet impulse for axon transmission would be calculated with the Fourier series analysis method based upon the mathematical function description of the data packet impulse.

[0035] Definitions of Cable (Axon) Impedance and Structural Return Loss in the most general terms are respectively: (1) cable (Axon) impedance is the ratio of the voltage to current of a signal traveling in one direction down the cable. In coaxial cable (Axon), the value of the impedance will depend upon the ratio of the inner and outer conductor diameters, and the dielectric constant of the material between the inner and outer conductors. The value of the conductivity will affect the impedance to the extent that RF signals (Data packet impulses) do not travel on the surface of the conductor, but propagate into the conductor by what is known as the skin depth. The finite conductivity also causes losses that increase with RF frequency (Data packet impulses' Fourier series), and this can change the effective cable impedance. Finally, (2) the construction of the cable (Axon) can change along the length of the cable (Axon), with differences in conductor thickness, dielectric material and outer conductor diameter changing due to limitations in manufacturing. Thus the cable (Axon) impedance can vary along the length of the cable (Axon). The extent to which the manufacturing imperfections degrade cable (Axon) performance is characterized by the specification Structural Return Loss (or SRL). Structural return loss is the ratio of incident signal to reflected signal in a cable (Axon) and has a linear relationship to effective data rate/speed. This definition implies a known incident and reflected signal. In practice, the SRL is loosely defined as the reflection coefficient of a cable (Axon) referenced to the cable (Axon)'s impedance/data packet speed. The reflection seen at the input of a cable (Axon), which contributes to SRL, is the sum of all the tiny reflections along the length of the cable (Axon). In terms of cable (Axon) impedance, the SRL can be defined mathematically as: ρSRL(ω)=eq. 1 Zin (ω)−Zcable (Axon) Zin (ω)+Zcable (Axon) Zin is the impedance seen at the input of the cable (Axon), and Zcable (Axon) is the nominal cable (Axon) impedance. Cable (Axon) impedance is a specification that is defined only at a discrete point along the cable (Axon), and at a discrete frequency. However, when commonly referred to, the impedance of the cable (Axon) is some average of the impedance over the frequency of interest. Structural return loss, on the other hand, is the cumulative result of reflections along a cable (Axon) as seen from the input of the cable (Axon). The above definitions need to be expressed in a more rigorous form in order to apply a measurement methodology. One definition of cable (Axon) impedance is that impedance which results in minimum measured values for SRL reflections over the frequency of interest (Data packet impulse via Fourier series). This is equivalent to measuring a cable (Axon) with a return loss bridge that can vary its reference impedance. The value of reference impedance/data packet speed that results in minimum reflection, where minimum must now be defined in some sense, is the cable (Axon) impedance. Mathematically, this is equivalent to finding a cable (Axon) impedance Zcable (Axon) such that: eq. 2 ∂[ρ(ω, Zcable (Axon))]∂(Zcable (Axon))=0 where ρ(ω) is some mean reflection coefficient. Thus, cable (Axon) impedance and SRL are somewhat inter-related; the value of SRL depends upon the cable (Axon) impedance, and the cable (Axon) impedance/data packet speed is chosen to give a minimum SRL value. An alternate definition of cable (Axon) impedance is the average impedance presented at the input of the cable (Axon) over a desired span. This can be represented as Zavg=eq. 3 Fmin∫Fmax Zin (ω)dω2π(Fmax−Fmin) The value found for Zavg would be substituted for Zcable (Axon) in equation (1) to obtain the structural return loss from the cable (Axon) impedance measurement. Any discourse on cable (Axon) measurements should include a discussion of the unique qualities of cable (Axon)s that make measurements so challenging. Because cable (Axon)s are electrically very long, and very low loss, the effect of any periodic defect in the cable (Axon) will be greatly multiplied. (2) Periodic faults and SRL where SRL is a reflection of incident energy that is caused by disturbances (bumps) in the cable (Axon) which are distributed throughout the cable (Axon) length. These bumps may take the form of a small dent, or a change in diameter of the cable (Axon). These bumps are caused by periodic effects on the cable (Axon) while in the manufacturing process (or myelination process). For example, consider a turn-around wheel with a rough spot on a bearing. The rough spot can cause a slight tug for each rotation of the wheel. As the cable (Axon) is passed around the wheel, a small imperfection can be created periodically corresponding to the tug from the bad bearing. Each of these small variations within the cable (Axon) causes a small amount of energy to reflect back to the source due to the non-uniformity of the cable (Axon) diameter. Each bump reflects so little energy that it is too small to observe with fault location techniques. However, reflections from the individual bumps can sum up and reflect enough energy to be detected as SRL. As the bumps get larger and larger, or more of them are present, the SRL values will also increase. The energy reflected by these bumps can appear in the return loss measurement as a reflection spike at the frequency that corresponds to the spacing of the bumps. Discrete cable (Axon) faults and SRL Reflections from faults within the cable (Axon) will also increase the level of SRL measured. The energy reflected from a fault will sum with the energy reflected from the individual bumps and provide a higher reflection level at the measurement interface.

[0036] The brain operates as a mesh network utilizing the multiple ends of its singular axon to interface via synapses to multiple neurons. A mesh network is a network topology in which each node relays data for the network. All mesh nodes cooperate in the distribution of data in the network. Mesh networks can relay messages using either a flooding (One-way Broadcast) technique or a (Transmit/receive routing) technique. With routing, the properly addressed message is propagated along a path by hopping from node to node (neuron to neuron) until it reaches its proper addressed destination. The address associated with the “Data packet impulse” must be assumed to be encoded via the shape of the “Data packet impulse”. To ensure all its paths' availability, the network must allow for continuous connections and must reconfigure itself around broken paths, using self-healing algorithms such as Shortest Path Bridging. Self-healing allows a routing-based network to operate when a node breaks down or when a connection becomes unreliable. As a result, the network is typically quite reliable, as there is often more than one path between a source and a destination in the network. A mesh network whose nodes (neurons) are all connected to each other is a fully connected network. Fully connected wired networks have the advantages of security and reliability ie. problems in a single cable affect only the two nodes attached to it. However, in such networks, the number of cables, and therefore the cost, goes up rapidly as the number of nodes increases. Fortunately, the human brain's 100 billion plus neurons and associated axons and dendrites form the most complex “known to man” mesh network for the costs of two humans' love, desire to procreate and their patience to raise the freshly constructed brain mesh network owner(s). The patience part may be the most interesting! With the complexity of the brain's mesh network of neuron/axon/dendrite connections, it is obvious that either an occasional or a continuous and massive internal generation of reflected duplicate addressed data packets from a strategically but, unfortunately positioned axon defect produces the overwhelming data packet flow consisting of the rogue “duplicate” message packets flowing from one neuron to the next to find its destination for the second, third or numerous times plus the properly addressed message packets that maintain the only portion of reality that the patient of schizophrenia has to hold on to.

[0037] Prior art research of the neurological medical community has produced an understanding that schizophrenia is a developmental disorder that involves abnormal connectivity. The evidence is overwhelming. Doctors have always wondered why schizophrenia typically develops during adolescence. Recall that adolescence is the period when the forebrain is being myelinated. The neurons there have been established, however, the myelin of the neurons' axons is still in the formative stages. Prior art studies by the neurological medical community have concluded that axons are abnormal (possessing fewer oligodendrocytes than normal) in several regions of the schizophrenic brain. Also, the prior art studies discovered that many mutated or damaged genes linked to schizophrenia were involved with myelin formation. Axon abnormalities have also been found in people affected by ADHD, bipolar disorder, language disorders, autism, dyslexia, tone deafness and others. Cognitive function depends on neuronal communication across synapses in the cortex's gray matter, where most psychoactive drugs act to diminish the symptoms of schizophrenia. Optimal communication among brain regions, depends on the axonal matter connecting the regions without any disruptions or confusion resulting from extraneous data flow. It has been found in prior art studies that disruption of genes in oligodendrocytes causes striking behavioral changes that mimic schizophrenia. The behavioral effects involve one of the same genes, neuregulin, found to be abnormal in biopsies of schizophrenic brains. The method of schizophrenia and other defective axon myelination related mental illness repair is accomplished by first examining and determining that the patient's genome (techniques involving isolation and amplification of DNA from whole blood samples and detection/confirmation of specific single nucleotide polymorphisms (SNPs) in the nrg1 gene. These polymorphisms represent DNA base-pair mutations or defects that can comprise coding (exon) or non-coding (intron) regions of any of the many isoforms of the multiply-spliced nrg1 gene product. These SNPs can be known or derived, and can be based on prior art knowledge or future research. All SNP targets shall be known or suspected of disrupting typical neuregulin splicing, expression, dysregulation, folding, function, or transport. Similarly, transcribed RNA can be isolated from whole blood or separated cell types, amplified via reverse-transcriptase polymerase chain reactions (RT-PCR), and probed for mutations (SNPs), deletions or insertions in the nrg1 gene via direct DNA probe hybridization or sequencing techniques.) contains a defective neuregulin expressing gene; second confirming neuron axon defective condition by measuring the electrical impedance (via measurement of the “Data packet impulse” speed which represents the axon health magnitude of the neuron region tested along the long axons between the left and right hemisphere neurons) of the outer myelin sheath to detect and locate regions of the brain where one or more defects are within the outer myelin sheath, thirdly repairing the neuron region of outer myelin sheaths via replacing damaged DNA neuregulin protein producing genes with (gene therapy and integration techniques such as correction of the nrg1 mutation or defect via the CRISP/Cas9 genomic editing system; insertion into the patient genome of a functional/typical nrg1 gene via vector (i.e., replication-deficient retroviral vector); or therapeutic supplementation of a corrected nrg1 coding sequence into targeted cell types that allows for the transient or long-term extrachromosomal expression of a functional nrg1 gene product (delivered via vectors such as genetically modified and/or pseudotyped Adenovirus, Adeno-associated virus, Herpesvirus, Retrovirus, Lentivirus, or Vaccinia virus), fourthly allow a healing period where the replaced brain region genes express the neuregulin proteins which construct uniform thickness myelin sheaths over the regional neuron axons repairing one or more defects in the outer myelin sheath with one or more of a protein and a lipid such that affected regions of neurons' outer myelin sheath regains the substantially constant electrical impedance for the normal transmission of data energy between the neurons, fifthly and subsequently measuring the electrical impedance via data packet speed of the outer myelin sheath to confirm the regained substantially constant electrical impedance for the transmission of the data energy between the neurons, wherein the first measuring and the subsequent measuring comprise determining differential electrical structural return losses (SRL)s of the axon indicating successful repair of the affected brain neuron region.

[0038] This novel process and method to prevent and or cure schizophrenia and other mental illnesses may be accomplished by detecting the abnormal or damaged gene(s), neuregulin and other associated genes, of the schizophrenia patient or even scan young people for the abnormal or damaged myelination gene(s), neuregulin and other associates genes, test/verify the “Data packet impulse packet” under speed, utilize gene splicing and or other gene correcting methods to put into place and activate the newly installed proper gene(s) to produce the proper proteins for the memory dendrite paring and final and proper axon myelination, allow time for the proper neuregulin gene myelination action and test/verify the correcting of the axon myelination by “Data packet impulse” speed registration.

[0039] Although the present invention is illustrated and described herein with reference to preferred embodiments and specific examples thereof, it will be readily apparent to those of ordinary skill in the art that other embodiments and/or examples may perform similar functions and/or achieve like results. All such equivalent embodiments and examples are within the spirit and scope of the present invention, are contemplated thereby, and are intended to be covered by the following non-limiting claims.