Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.
Neuropyrosis
Receptive Quotient and its
role in Alzheimer’s Disease
By Anand Madhu (Droog)
Abstract
THE NEUROPYROSIS THEORY OF AD
1) As we all know, the two psychological chemicals in the brain are Dopamine (the c...
Abstract
Why?
There is too much dopamine in brains that lack sufficient Norepi.
[link to en.wikipedia.org]
"The loss of no...
Alzheimer’s Disease (AD)
– “Deter showed symptoms like loss of memory and delusions. She would have
trouble sleeping, woul...
The DLMS & the NLMS
Seeing the Dopamine-Linked and
Norepi-Linked Micro-Systems as the
Logic Gates of the Nervous System
• The brain’s roughly 1011 neurons are randomly connected by roughly 1014 interneuron
connections (synapses)
• The dendrit...
The Dopamine-linked Micro-system
Axon terminal (say)
Nearly all the
images found
in this work
were found
online, a BIG
THA...
Dopamine (D) & Norepi (N)
• Dopamine (D) & Norepi (aka Norepinephrine aka Noradrenaline aka
N), whose micro-systems reside...
DLMS and NLMS work by boosting Signals
• As signals march through the brain, they either weaken and fade away, or
are boos...
Conventional wisdom regarding neuron functionality
Traditionally, it has been known that dendritic spines collect electric...
Sheffieldian information flow/signal transmission
However, “Sheffield et al. assert that some action potentials began at t...
Monoconditional signalling Multiconditional signalling
DLMS/Dopamine’s NLMS/Norepi’s
How do the DLMS and the NLMS work?
Monoconditional signalling Multiconditional signalling
Red line denotes incoming signal
DLMS’s NLMS’s
Signal incoming
Weak...
Monoconditional vs. Multiconditional signalling
• In Monoconditional signalling, boosting activity
occurs on the (generall...
Monoconditional vs. Multiconditional signalling
Monoconditional signalling Multiconditional signalling
Blue line = boosted...
Memory – an example of Dopaminic boosting
• One of the simplest
forms of receptive
boosting is found in
dendritic memory…
...
(1) Dendritic conventional/axon hillock-type aka Receptive transmission
(2) Axonic Sheffield mechanism aka Generative tran...
Summary – 2: Logic Gates of the CNS
• Electronic circuits are an analogy to understand how D-gates (DLMSs)
and N-gates (NL...
• Thus the brain can be defined as a package of many parallel processing networks
(circuits)... each circuit is made up of...
RQ (Receptive Quotient/Dopaminic Quotient)
• Certain behaviors involve more NLMSs/Norepi
– E.g.: Logical talent, that is b...
Identifying RQ as “behaviors which involve a
quantitative dependence on external stimuli”
 A general law to identify RQ-t...
• If one understands how high-RQ people follow
what’s in other's minds -- he will see why they --
unlike the low-RQ people...
More examples to illustrate the RQ-based lifestyle
• Generally speaking, high-RQ people are more expected to have a quanti...
Are we on the right track?
 Empirically, we see that RQ-type behavior occurs less in the white matter/Norepi-
heavy class...
• One needs a very high RQ to
effectively make the “laws of
power” a part of daily life, as
their practice generally
invol...
Neuropyrosis (‘overheating of neurons’)
• The Neuropyrosis theory of dementias carries 4 statements
which will be proven:
...
a.) Norepi/NLMS/Axon deficiency (which is nothing but
excessiveness of Dopamine/DLMSs/dendrites) is possible
• In a separa...
A weak Norepic system is suggested by
Dopamine-beta-hydroxylase deficiency
• “Dopamine-beta-hydroxylase deficiency is a co...
• “According to one study by the NIH, 100% of
individuals [with Norepinephrine deficiency]
studied suffered severe orthost...
b.) Dopamine is alien in the upper brain
• "The prefrontal cortex is one of the very few cortical areas to receive a dopam...
• Nearly half the body’s dopamine is outside the brain (governing linear processes
which need only its monoconditional sig...
 In the upper brain, increased activity of Dopamine and decreased activity of
Norepi (reduced white matter and/or increas...
d.) Alzheimer’s Disease in a very Dopamine-
dependent neurocircuital/structural ideology
• Due to quite a few reasons (e.g...
How can excessive Dopamine activity be
associated with AD? – The Neuropyrosis Theory
 A high RQ brain, in which D is exce...
• In the ancient computers using vacuum tubes, as Tony Stockill says,
“with each tube generating heat to work, the cooling...
Thus there are 2 types of brains;
in type A
there are, say, something like a trillion Norepi and 6 trillion Dopamine
check...
Confirming the greater signal density in AD
• The increased energy/signal density (which is, evidently, due to more dopami...
The Neuropyrosis Theory of AD
• A highly quantitative presence of signals is a devastating thing for brain
tissue.
– Each ...
Thus, just how a piece of
polystyrene rapidly shrinks
if exposed to fire, or how
the plastic covering of an
electrical cab...
Depression
• Dementias are bad by themselves, but what’s worse is that budding patients also
seem to suffer depression.
• ...
––––– References––––––
• (1) Burgess, P. W., Veitch, E., & Costello, A. (submitted). The role of the right rostral prefron...
• (19) Derflinger S et al. (2011), Grey-matter atrophy in Alzheimer's disease is asymmetric but not lateralized., J
Alzhei...
Upcoming SlideShare
Loading in …5
×

Receptive Quotient and its Role in Depression and Dementia

1,652 views

Published on

The hitherto-unknown culprit behind stress, depression, and Alzheimer’s Disease is finally exposed!

Published in: Lifestyle, Technology, Business
  • Be the first to comment

Receptive Quotient and its Role in Depression and Dementia

  1. 1. Neuropyrosis Receptive Quotient and its role in Alzheimer’s Disease By Anand Madhu (Droog)
  2. 2. Abstract THE NEUROPYROSIS THEORY OF AD 1) As we all know, the two psychological chemicals in the brain are Dopamine (the chemical which corresponds more to gray matter) and Norepi, the chemical that corresponds more to white matter (“Psychological”, or quantum-psychological, in the sense of how both engage in signal- transmutation behavior. But Dopamine engages in one-to-one transmutation; Norepi engages in a many-to-one transmutation, as shown elsewhere in this thesis) 2) All neural circuits are comprised of Dopaminergic and Norepic "work stations", which can be likened to logic gates. 3) Depending on genes/environment*, any man's neural circuits tend to use either more Dopaminergic, or more Norepic work stations. (*Digression: In particular, the modern day's dominant analytic tradition, aided possibly by unhealthy habits (sugar intake etc.), may encourage a more Dopamine-oriented "education" and "growth" of the brain) 4) If more Dopaminergic work stations are present; if a man's neurostructural ideology is more Dopamine-based – it translates into a higher electric/signal density in the brain, which leads to overheating of the brain, causing AD by what I call the "neuropyrosis" (literally "fire in the brain") process.
  3. 3. Abstract Why? There is too much dopamine in brains that lack sufficient Norepi. [link to en.wikipedia.org] "The loss of noradrenergic [Norepic] neurones is a striking feature of sporadic Alzheimer's disease (AD)." [ [link to www.biomedcentral.com] So, in a nutshell, there are 2 types of brains; In type A there are, say, a trillion Norepi and 6 trillion Dopamine check posts; In type B there are, say, half a trillion Norepi and 100 trillion Dopamine check posts; See, the dopamine or the Norepi molecule adds an equal amount of electrical energy. So in type B brains, there is greater signal density, one can generally say, which leads to overheating, causing localized ‘neuropyrosis’ events manifesting ultimately as dementia. In the following thesis, the above theory is substantiated and discussed at length.
  4. 4. Alzheimer’s Disease (AD) – “Deter showed symptoms like loss of memory and delusions. She would have trouble sleeping, would drag sheets across the house, and scream for hours in the middle of the night”. – Dementia means “without mind”. Alzheimer’s Disease is “characterized by loss of neurons” (brain cells). – “AD can progress undiagnosed for years”. – “Growing impairment eventually leads to diagnosis.” Even though AD is typically undiagnosed, diagnosed AD is common: 1 in 10 over 65, 1 in 2 over 85, suffer AD! – Heidi Evans quotes a report from the Centers for Disease Control which shows that "1 in 3 senior citizens now dies with Alzheimer's disease“, and “Alzheimer’s deaths have increased 68% from 2000 to 2010, while deaths from other major diseases such as heart disease, stroke and breast cancer have all declined". – Apparently, human lifespan is up to 120 years, but Alzheimer’s dementia cuts it short. – This meta-thesis explores the cause of Alzheimer’s Disease or other dementias
  5. 5. The DLMS & the NLMS Seeing the Dopamine-Linked and Norepi-Linked Micro-Systems as the Logic Gates of the Nervous System
  6. 6. • The brain’s roughly 1011 neurons are randomly connected by roughly 1014 interneuron connections (synapses) • The dendrites and axons act as signal cables, forming paths that transmit information in the form of electrical signals (whether a particular path signals or not is in itself the information… rather than information being “encoded” as signals which are modulated) • Below: a neuron linked to a “transport axon”, which brings in visual information from the Eye Just how leaves pick up light, a dendrite’s spine picks up travelling signals *(a path, i.e. a chain of signal cables, actually… terminating in a (transport) Axon)*
  7. 7. The Dopamine-linked Micro-system Axon terminal (say) Nearly all the images found in this work were found online, a BIG THANKS to their creators
  8. 8. Dopamine (D) & Norepi (N) • Dopamine (D) & Norepi (aka Norepinephrine aka Noradrenaline aka N), whose micro-systems reside in/around the dendrite and axon respectively, are the two most important chemicals in the brain (i.e., in the psychological frame of reference – a claim that will be proven) • The systems within which they act – may be called the Dopamine- linked Micro-system (DLMS) & Norepi-linked Micro-System (NLMS) • The N/D-LMSs have signal-modification-related (i.e. “quantum psychological”) roles – which are, for now, more interesting than their physiology. • How do D and N work? • D and N are structurally and functionally similar. They both work by boosting (valid) signals. Dopamine Norepi
  9. 9. DLMS and NLMS work by boosting Signals • As signals march through the brain, they either weaken and fade away, or are boosted/amplified. • This boosting/amplification is the role of the DLMS/NLMS; of this boosting characteristic, it is said: – "Intracortical currents are triggered by the release of neurotransmitters” – “neuromodulators like noradrenaline, dopamine or serotonin have indirect modulating effects" - Frodl-Bauch et al., 1999, as quoted in Nieuwenhuis (12). – They “enhance the synaptic responses of cortical neurons... increasing the gain of cortical neuronal activity”, thus N “serves to amplify signal conduction" (Nieuwenhuis, 12).  Similar is the role of DLMS, since D and N are structurally and thus functionally similar • Thus these neurotransmitters boost/amplify valid signals. • The DLMS and NLMS have different manners of boosting signals, as seen in my research here. • To summarize my research: the DLMS carries out what is called monoconditional signalling, and the NLMS carries out multiconditional signalling.
  10. 10. Conventional wisdom regarding neuron functionality Traditionally, it has been known that dendritic spines collect electric signals, after which these signals add up cumulatively, and are relayed further by axons, as shown in the picture on the right. This is the mechanism upon which the “perceptron” neural networks are based. But we can only call them semi-neural networks. For you see, Sheffield has discovered a new, Axon-centric type of Signalling covered in the next page. (Conventional type flow of information )
  11. 11. Sheffieldian information flow/signal transmission However, “Sheffield et al. assert that some action potentials began at the distal end of the axon (the end not connected with the cell body) instead of at the axon hillock”, and consequently, that “axons can communicate with each other without the signal first going through dendrites or cell bodies.” The presence of the NLMS explains this unconventional, axon-centric type of transmission. Note: However, it appears that, even in this (Sheffieldian) case, there are signals in the dendrital side, albeit they are perhaps small and consequently, not easily measurable. The reason for saying this is that what I call (a bit confusingly, I admit – sorry for that) an “Axonic” neuron’s axonal elaboration is accompanied by more “higher order1” dendrital elaboration, as Chatham notes, saying: “The left hemisphere2 has larger dendritic branching than the right hemisphere, but only at large distances from the dendrite’s main shaft -- the opposite trend holds at distances closer to the main dendrite” [so the axonal neurons of the right hemisphere have more “higher- order” dendrital branching; it seems like a Sheffieldian-firing oriented neuronal design which we term as axonic]. 1 I later found out that what I call “higher order” is, among some academics, called “lower order” – thankfully it is a merely nomenclatural detail that doesn’t matter 2 In the left hemisphere, axonal elaboration is generally lesser, and the opposite trend holds for the right hemisphere
  12. 12. Monoconditional signalling Multiconditional signalling DLMS/Dopamine’s NLMS/Norepi’s How do the DLMS and the NLMS work?
  13. 13. Monoconditional signalling Multiconditional signalling Red line denotes incoming signal DLMS’s NLMS’s Signal incoming Weak signals come and switch on all signal traps associated with the NLMS’s task cycle. How do the DLMS and the NLMS work? Axon fires only when all 3 (or n, more generally) signals are present. Thus it engages in a sort of selective, AND-gate-like firing (more than 1 stimuli must exist for Axon to fire). This conclusion is supported by how the cone, which is analogous to the axon, engages in selective processing (“require more light [than rods] to detect images”).
  14. 14. Monoconditional vs. Multiconditional signalling • In Monoconditional signalling, boosting activity occurs on the (generally dendritic) dendrital side, which is more likely “closer” to external stimuli (see also dopamine’s stimuli-responsive nature); so we call it Receptive signalling activity Dopamine-linked-Micro- system-aided boosting activity Norepi-linked-Micro- system-aided boosting activity DLMS’s NLMS’s Monoconditional signalling Multiconditional signalling back • In Multiconditional signalling, boosting activity occurs on the Axonal side; it may be called Generative signalling activity even though the sources of the initial signals are on the dendrital side (these dendrites can usually be called axonic) Generative activity = Sheffield type signalling Receptive activity = Typical stimuli responsive signalling
  15. 15. Monoconditional vs. Multiconditional signalling Monoconditional signalling Multiconditional signalling Blue line = boosted (stronger) signal advances On the right, the number 3 is chosen arbitrarily. It is more correctly n, where n>1. DLMS’s NLMS’s
  16. 16. Memory – an example of Dopaminic boosting • One of the simplest forms of receptive boosting is found in dendritic memory… • Complex forms are found in RQ-type behavioral circuits… • Memory example: A small aspect of an object (data about which is stored), is recalled – that step reflects an input signal which, upon several boosting operations, causes, in its turn, the recollection of the object in its entirety The term “Receptive” depicts the DLMS’s type of activity, due to how it exhibits a linear receptiveness to (that is, boosting of) incoming signals Memory 1 Memory 2
  17. 17. (1) Dendritic conventional/axon hillock-type aka Receptive transmission (2) Axonic Sheffield mechanism aka Generative transmission Summary: 2 modes of boosting-aided transmission A B C D A B C D •Signal strengths at various sites are, for example: •This is the DLMS-guided mode of transmission and, being away from the soma and more originating in spines, it can be defined as relatively more reactive to stimuli (receptive). •The axon transmits signal because the sheer strength of the signals coming from, say, C and D – rams the signal through E in the “action potential” method – the axon doesn’t fire “of its own will”, using the Sheffield mechanism; axon merely serves as a signal cable… •Signal strengths at various sites are, for example: A: weak B: weak C: weak D: strong •This is the NLMS-guided mode of transmission. •The axon fires because the NLMS feels (somehow) the weak dendritic signals at A, B and C…. the axon fires “of its own will”, through E. Axon is also a detector, not a mere signal cable E Chris Chatham observes that the left hemisphere has larger dendritic branching than the right, at large distances from the dendrite’s main shaft, and the opposite trend holds at distances closer to the main dendrite. Thus, if axon terminals are more developed (e.g.: right hemisphere, or more generally in “white matter”), there is more branching closer to the soma, which supports the above diagram’s observation…. A: weak B: weak C: strong D: strong E: strong
  18. 18. Summary – 2: Logic Gates of the CNS • Electronic circuits are an analogy to understand how D-gates (DLMSs) and N-gates (NLMSs) are variously permuted, to form neural circuits which variously process information Artificial logic gates A B C Output 0 0 0 0 0 0 1 0 1 0 0 0 0 1 0 0 1 1 0 0 0 1 1 0 1 0 1 0 1 1 1 1 A Output 0 0 1 1 Natural logic gates
  19. 19. • Thus the brain can be defined as a package of many parallel processing networks (circuits)... each circuit is made up of Dopaminic and Norepic signalling apparatuses Summary – 3: A package of many parallel circuits The neural correlates of RQ (example)
  20. 20. RQ (Receptive Quotient/Dopaminic Quotient) • Certain behaviors involve more NLMSs/Norepi – E.g.: Logical talent, that is better called “theoretical logical talent”, requires more Norepi’s context-sensitive/qualitative associative style of working, than Dopamine’s quantitative associative style, as seen here. • Other behaviors involve more DLMSs/Dopamine – E.g.: Syllogistic talent (“analytical logical talent”) – memorization/ recall in the “rote” tradition -- is a behavior where DLMSs are used more. • “RQ” (Receptive Quotient) is an umbrella term for behaviors which involve neural circuits with more DLMSs.
  21. 21. Identifying RQ as “behaviors which involve a quantitative dependence on external stimuli”  A general law to identify RQ-type circuits is that such circuits are quantitatively dependent on external stimuli, reflecting a dendritic, DLMS- heavy structural ideology. 1. Example of an RQ circuit -- in Obsessive Compulsive Disorder, the person is responding to a large quantity of dirt particles, which is the quantitative external stimuli that we must look for, in determining whether or not “more DLMSs” are involved ). 2. When you see people reacting to a large quantity of superficialities (having a quantitative mode of function) instead of dealing with a few core matters (a qualitative mode of function) – it is an external stimuli-reactive mode of functioning, involving more of a DLMS component; and the “absent-minded professor” is the opposite! 3. The serial killer, before finalizing his target, checks a lot of things – whether or not anyone is nearby, whether or not all doors and windows are closed, whether or not a road is nearby, whether or not a spare set of clothes is available and so on; an external stimuli-oriented way of functioning so likely involving more DLMSs. 4. Verbal (quantitative) theory of mind quantitatively registers what is in other peoples' minds (which is external stimuli), for later usage in solution- fetching -- this faculty is very different from the Empath’s qualitative Theory of Mind
  22. 22. • If one understands how high-RQ people follow what’s in other's minds -- he will see why they -- unlike the low-RQ people called “Aspergians” -- are quicker in understanding the below cartoon -- Quantitative/verbal-based ToM (*not to be confused with the “Qualitative ToM” mechanisms found in “Empaths” and many Negros) • or why high-RQ people may say “Sally will look for the ball in the basket”… as they are somewhat prone to memorizing (and living off) false beliefs – because remembering false beliefs was useful in the craft of solution-fetching, the RQ-linked opposite of IQ-linked problem-solving The ‘Sally Anne test’ is used to differentiate Aspergian and “normal” children
  23. 23. More examples to illustrate the RQ-based lifestyle • Generally speaking, high-RQ people are more expected to have a quantitative neural lifestyle, rather than a qualitative one; thus they’re more likely to subscribe to the quantitative external stimuli-oriented policies laid out by Robert Greene in "48 laws of power”:-
  24. 24. Are we on the right track?  Empirically, we see that RQ-type behavior occurs less in the white matter/Norepi- heavy class of people called “Aspergians”, and more in grey matter/Dopamine-heavy people.  For example, Eric Michael Johnson cites about “a clear, linear relationship between the size of a monkey’s social network and an increase of neocortical gray matter in regions involved with social cognition”.  Thus, relating such quantitative social activity to gray matter or Dopamine, and RQ, seems the right thing e.g.: researchers found that "Fruit flies that are "socially stimulated" have three times the amount of dopamine in their brains than "socially deprived" fruit flies" (Indrani et al.). • Note: We call for qualitative as opposed to quantitative1 social activity, not the cessation of social activity.  Similarly: – "Early Social Experience Is Critical for the Development of Dopamine Modulation of Prefrontal Cortex Function (Petra et al.)".  And: – "increased social status and support correlated with the density of dopamine D2/D3 receptors" (Martinez et al.). • Clearly, quantitative social interaction is linked to a heavily-DLMS-based structural ideology. • Heavily DLMS-involving/quantitative signalling-involving mental activities are: syllogistically-based (thus quantitative1) calculative lifestyles e.g.: money or stock-chasing, usual corporate matters: ‘cut-throat’ competitionism, “game theory”- based lifestyle etc. – 1: Logically-based mental lifestyles are, in contrast, qualitative (involving qualitative rather than quantitative signalling), partly since they are optimized and therefore involve less mental processing.
  25. 25. • One needs a very high RQ to effectively make the “laws of power” a part of daily life, as their practice generally involves quantitative caches of external stimuli and memories that are additively processed by the linear thinking faculty:  DLMS usage in linear thinking: • A major user of DLMSs is syllogical faculty or the more general linear thinking faculty, which has traditionally been identified as “left brain logic”. • It is an associative talent centered about the dendritic LT-area • Syllogic is mainly about two things: firstly memorization and recall, and secondly syllogistic association of verbal “meanings” to form further statements and “meanings”... • Syllogic is identified with the “analytic” branch of western philosophy
  26. 26. Neuropyrosis (‘overheating of neurons’) • The Neuropyrosis theory of dementias carries 4 statements which will be proven: a. Norepi/NLMS/Axon deficiency (which is nothing but excessiveness of dopamine/DLMSs/dendrites) is a feasible pathology b. Dopamine can almost be called “alien” in the (upper) brain, an organ that originally was, primarily, the home turf of Octopamine (and later, Norepi) ever since the evolution of brain in the animant (as covered in Paper B, the New Thesis)... c. The Dopaminergic system is expansionistic in the upper brain  It seems Dopaminergic and Noradrenergic Innervaters “drift” across areas of the brain, settling down* wherever calculative circuits/memories must be formed. * In quasi-Lamarckian (characteristics acquired during lifetime), Lamarckian (characteristics passed down to children), and Darwinian styles (characteristics acquired over generations)… d. A NLMS-deficient/hyper-DLMS neurostructure is associated with depression and Alzheimer’s disease, which may arise due to overheating
  27. 27. a.) Norepi/NLMS/Axon deficiency (which is nothing but excessiveness of Dopamine/DLMSs/dendrites) is possible • In a separate thesis, I compare Axons, cone cells, and Fungiform papillae, which are similar microsystems in having Norepi at their calculative hearts. If deficiency of cones is possible – • “The most usual cause of color blindness is a fault in the development of retinal cones” • “Destruction of the cone cells from disease result in blindness.” – and deficiency of Fungiform papillae is possible – • Fukutake et al. speak of “Absence of fungiform papillae on the tongue”… (and other hypo-GS/hyper-RS symptoms : “Sural nerve biopsy demonstrated a marked loss of myelinated fibres [axons/white matter] and a reduction in the number of unmyelinated axons”… “Neuro-imaging studies revealed atrophy of the spinal cord, cerebellum, brainstem and corpus callosum, and enlargement of the lateral, third, fourth ventricles.”) – then certainly deficiency of Axons is also possible. Indeed, it is called “white matter disease”: • Dr. Nicole Anderson: "Our findings add to a growing body of evidence that white matter disease is a discreet saboteur in the brain, impacting a large number of cognitive functions. It is responsible for about a fifth of all strokes worldwide (Sudlow, 1997), more than doubles the future risk of stroke (Debette 2010, Vermeer, 2007), and is a contributing factor in up to 45% of dementias (Gorelick, 2011).” The prevalent view is based on an “evil, villainous disease” idea, saying: “white matter disease is a mind-robbing condition that targets small blood vessels deep within the brain's white matter. The disease hardens the tiny arteries, gradually restricting nutrients to white matter” – but in fact the victim’s lifestyle/genes/environment, which results in less NLMS/axonic/white matter type processes, and more of the Dopaminic (RQ) – is in itself to blame. White matter withers away due to the “use or lose” law, even as grey matter declares its fiefdoms across the brain (leading to neuropyrosis events in hippocampus, PFC etc.)
  28. 28. A weak Norepic system is suggested by Dopamine-beta-hydroxylase deficiency • “Dopamine-beta-hydroxylase deficiency is a condition involving inadequate Dopamine-beta- hydroxylase. It is caused largely by [associated with] increased amounts of serum dopamine and release of dopamine in place of Norepinephrine; sometimes it is known as Norepinephrine deficiency”. • Researchers of depression, schizophrenia, and migraines are very interested in studying this disorder • It is associated with severe symptoms such as Ptosis of the eyelid (see picture), Prolactin deficiency (female’s inability to produce milk), and difficulty standing still for longer than one minute. • Another symptom is hypoglycemia – that is, abnormally diminished content of glucose in the blood (which may be because the their generally hyper-Dopaminergic System is quickly burning up carbohydrates – a high metabolic rate). Ptosis of the left eyelid (unilateral ptosis). An 1852 headshot daguerreotype by William Bell.
  29. 29. • “According to one study by the NIH, 100% of individuals [with Norepinephrine deficiency] studied suffered severe orthostatic hypotension, 80% suffered anemia, 43% epileptic symptoms, 100% nasal stuffiness, 33% suffered hypoglycemia, 60% frequent urination and nighttime frequent urination, 50% muscle hypotonia, 75% postprandial hypotension, and 100% suffered from sleep problems”. • Quoting part of the abstract of a very important 1981 paper by Cross et al.: “The activity of the enzyme dopamine-beta- hydroxylase was measured. Enzyme activity was decreased in the frontal and temporal cortices and hippocampus in patients with Alzheimer's disease. The decrease in enzyme activity in Alzheimer's disease may reflect abnormality of cortical noradrenergic fibres.” Norepinephrine Deficiency A Brazilian girl with Ptosis, c.1870.
  30. 30. b.) Dopamine is alien in the upper brain • "The prefrontal cortex is one of the very few cortical areas to receive a dopaminergic innervation" (Bruin et al.). • The upper brain is the natural ecology for Norepi – it can be plainly inferred from how Norepi travels farther (right), has a greater range of operation across the brain – as opposed to Dopamine (left), whose regions of operation are limited... Range of Dopamine Range Of Norepi * All the RQ type behaviors which we have studied, are partially handled by Dopaminergic modulative areas in the Prefrontal Cortex (PFC), where an excessive role as controller played by D, as in high RQ people, is anomalous *
  31. 31. • Nearly half the body’s dopamine is outside the brain (governing linear processes which need only its monoconditional signalling) – is excessive Dopamine (D) in the brain, a risk? • Presence of D in some regions of the brain is “anomalous”, e.g.: the prefrontal cortex, which Morón et al. describe as a “region with low levels of the dopamine transporter” (DAT). • Morón et al. note: “In the striatum and basal ganglia, dopamine is inactivated by reuptake via the DAT. In the prefrontal cortex, however, there are very few DAT proteins, and dopamine is inactivated instead by reuptake via the Norepinephrine transporter” (17). • A cuckoo characteristic – is prefrontal D in a calculative (RQ) role owing to complex sub-Norepic substrates? • The PFC benefits availed to D are covered by Yavich et al. (18): “The DAT pathway is an order of magnitude faster than the NET pathway: in mice, dopamine concentrations decay with a half-life of 200 milliseconds in the caudate nucleus vs. 2,000 milliseconds in the prefrontal cortex.” • Thus though the lower brain (caudate nucleus etc.) is Dopamine’s natural home, we cannot say that for the upper brain (i.e., prefrontal cortex and its backyard, where increased entrenchment of Dopamine, as in high RQ people, may be linked to problems). • On the basis of b.), may theorize: problems may arise due to general hyperactivity of Dopamine in the upper brain… as will be discussed in the “Neuropyrosis” theory b.) Dopamine is alien in the upper brain
  32. 32.  In the upper brain, increased activity of Dopamine and decreased activity of Norepi (reduced white matter and/or increased grey matter) – is associated with various mental disorders:  Hyper-Dopamine in PFC translates to Obsessive Compulsive Disorder ("Low level of dopaminergic D2 receptor binding" less binding means increased Dopamine activity) or Schizophrenia ("Schizophrenia: More dopamine, more D2 receptors")  Hypo-Norepi (Hypo-white matter) in a specific region translates to Psychopathy ("a white matter tract called the uncinate fasciculus, is disrupted in psychopathic individuals")  Hyper-Dopamine in brain (deficits in right brain), in general, translates to Non- verbal Learning Disability ("Brain scans of individuals with NLD often confirm mild abnormalities of the right cerebral hemisphere“, which is home primarily to N, and less so to D)  Hypo-Norepi (Hypo-white matter) in a specific region, the corpus callosum, translates to ACC/Kim-Peek Disorder ("complete or partial absence of the corpus callosum, the band of white matter")  Hyper-Dopamine in Frontal executive Network translates to Epilepsy ("Decreased Dopamine D2/D3-Receptor Binding in Temporal Lobe Epilepsy" -- decreased binding means increased activity") c.) The Dopaminergic system is “expansionist”
  33. 33. d.) Alzheimer’s Disease in a very Dopamine- dependent neurocircuital/structural ideology • Due to quite a few reasons (e.g.: Dopaminergic system’s expansionism, competition for similar adjunct chemicals (e.g.: how D occupies the NET pathway) due to structural/functional similarities of Dopamine and Norepi) – Dopamine and Norepi exist in a Yin-Yang relationship – i.e., excessive dopamine in the system generally implies a lower level of Norepi and vice versa*………………………………………….…………..(i) * For example, we see: “persons with Dopamine beta hydroxylase deficiency [Norepinephrine deficiency] have triple fold amounts of dopamine in their system”… others say “In this, there is a "five- to tenfold elevation of plasma dopamine"” [29].  Heneka et al. say: – “Alzheimer’s diseased individuals show ~ 70% loss of locus coeruleus (LC) cells” and – “Degeneration of the LC may be responsible for higher Aβ deposition in Alzheimer's disease.”  The locus coeruleus, a producer of Norepi, is correlated with levels of Norepi in the brain; hence Alzheimer’s disease is characterized by low levels of N*, and also, from (i), increased presence of Dopamine. * For example, we read, in “In AD, reductions in noradrenergic neurones within locus coeruleus, as well as reduced brain noradrenaline levels, have often been reported” (Lyness et al., 2003).  In other words: an overly DLMS-based, NLMS-deficient neurocircuital system – is linked to Alzheimer’s Disease.
  34. 34. How can excessive Dopamine activity be associated with AD? – The Neuropyrosis Theory  A high RQ brain, in which D is excessively present in a calculative capacity and/or there is more dendrital development (more development of grey matter i.e. mostly dendrites) – suffers damage due to overheating.  Why? A. The D-gate is the quantitative gate, the N-gate is the qualitative gate... and under-use of the qualitative gate causes big problems. In other words: – In a brain which is “abnormally” dependent on RQ-type circuits – there are too many DLMSs; as a relatively simplistic (monoconditional signalling), archaic (paper B) logic gate is being overused in the neurocircuital architecture. Just how olden electronic circuits used many more parts than new ones for similar jobs – an overly-DLMSs-based neurocircuital architecture also uses an order of magnitude more DLMSs
  35. 35. • In the ancient computers using vacuum tubes, as Tony Stockill says, “with each tube generating heat to work, the cooling problems were huge. Large blowers and cooling fans around the tubes, as well as air conditioning were standard. Liquid cooling was also used”. This ancient technology-based system generates more heat. • As he adds: “When transistors came along, there was less heat per circuit”. This modern technology-based system generates far lesser heat. • Human brains can be understood by that analogy – a brain which is largely dependent on dopamine-based processes, experiences more internal heat than a brain that is largely dependent on Norepi- based processes A simple analogy
  36. 36. Thus there are 2 types of brains; in type A there are, say, something like a trillion Norepi and 6 trillion Dopamine check posts; in type B there are, say, something like half a trillion Norepi, 100 trillion Dopamine check posts; Type A engages in qualitative signalling, type B in quantitative signalling  In type B brains, in a process whose volume is proportional to the number of check posts present, a very high number of gates are discharging their energies into the net signal volume  Since each D/N-LMS activity adds the same amount of energy, type B brain experiences an overall greater energy density.  Thus a brain which is largely based on DLMSs – generally experiences greater signal density. A simple analogy
  37. 37. Confirming the greater signal density in AD • The increased energy/signal density (which is, evidently, due to more dopamine logic gates – quantitative computation) in case of Alzheimer's disease, is discussed by Alice Walton of Forbes: – “People who have more activity in their default mode networks may have increased risk for Alzheimer’s disease. As D. Holtzman of Washington University says, “people whose default mode networks have an average increase in activity relative to others may be at increased risk to get Alzheimer’s disease later in life and less activity in this network, less risk” – The MPFC, a central part of the default mode network, is associated with more dendrites /Dopamine, as shown in paper D. • Note: The “Amyloid” debris associated with AD -- is particularly pronounced in the Dorsolateral PFC (Murray et al., 2012), where most of the RQ-related calculative neural tissues are found, and where Dopamine activity is (I theorize) “anomalous”. • The increased signal density in case of Alzheimer's disease is confirmed in how the lateral ventricles, which carry ventricular fluid to support neural activity by attending to metabolic waste, are enlarged in Alzheimer's disease; that once again indicates excessive signalling activity (Interestingly, the ventricles are enlarged also in bipolar disorder).
  38. 38. The Neuropyrosis Theory of AD • A highly quantitative presence of signals is a devastating thing for brain tissue. – Each time a signal passes through a dendrite, some loss occurs on the way. – This loss is converted to heat (the electrical equivalent of friction). – Greater energy/signal density implies, therefore, overheating – Overheating causes neuronal collapse and "neuroinflammation" (which is maybe a repair reaction) in areas: hippocampus (handles conceptualization), EC, PFC etc. • Effect of overheating due to excessive monoconditional signalling activity:
  39. 39. Thus, just how a piece of polystyrene rapidly shrinks if exposed to fire, or how the plastic covering of an electrical cable melts if too much direct current passes through it – hyper-signalling associated with the nature of hyper-D neurocircuital ideology – destroys the substrate (axons/dendrites).
  40. 40. Depression • Dementias are bad by themselves, but what’s worse is that budding patients also seem to suffer depression. • So we say since similar observations are made in depressed and demented brains: “Default mode network shows greater activity when depressed participants ruminate” (22). Further, Depression involves enlargement of lateral ventricles (23), like AD. • “Studies have shown that high concentrations of the neurotransmitter Norepi leads to feelings of elation and euphoria [extreme happiness] (Franken, 1994).” • Further we read, in Mental Health Daily: “When levels [of Norepi] are low, a person can lack motivation, healthy cognition, and intellectual skills – all of which are vital for success… Other evidence shows that when Norepinephrine is reduced in rats, they become inactive, have poor appetites, and are model aspects of depression”. • Conclusion: High RQ people are susceptible to depression and dementia, via the neuropyrosis mechanism • Conclusion: In the neuropyrosis-afflicted brain, the processes, in general, do not involve qualitative areas (like the NLT-area), and, therefore, quantitatively burden critical areas (e.g.: hippocampus) – which, like over-burdened marchers, might hold up the brain as a whole, leading to motivation deficit, fatalism, pessimism etc. The idea that a hyper-DLMS state causes Alzheimer's disease, is confirmed in how, "In Alzheimer's disease (AD), brain atrophy has been proposed to be left lateralized" (19) (more atrophy in the left hemisphere) – in the light of the detail that the left hemisphere, has DLMSs in majority, relative to the right hemisphere
  41. 41. ––––– References–––––– • (1) Burgess, P. W., Veitch, E., & Costello, A. (submitted). The role of the right rostral prefrontal cortex in multitasking: The six element test. • (2) Hongwei Liu et al. (2004), Isolation of Araguspongine M, a New Stereoisomer of an Araguspongine/Xestospongin alkaloid, and Dopamine from the Marine Sponge Neopetrosia exigua Collected in Palau • (3) Simon Weyrer et al., Serotonin in Porifera? Evidence from developing Tedania ignis, the Caribbean fire sponge (Demospongiae), Memoirs of the Queensland Museum 44: 659-665. Brisbane. ISSN 0079-8835. • (4) Mayer, AM (2006). "Polyphenol oxidases in plants and fungi: Going places? A review". Phytochemistry 67 (21): 2318–2331. • (5) Van Alstyne et al. (2006). "Dopamine functions as an antiherbivore defense in the temperate green alga Ulvaria obscura • (6) Schwaerzel M et al. (2003). "Dopamine and octopamine differentiate between aversive and appetitive olfactory memories in Drosophila“ • (7) Tang, F; Tao, L; Luo, X; Ding, L; Guo, M; Nie, L; Yao, S (2006). "Determination of octopamine, synephrine and tyramine in Citrus herbs by ionic liquid improved 'green' chromatography". • (8) Lutzenberger, W., Elbert, T., Rockstroth, B. (1987). A brief tutorial on the implications of volume conduction for the interpretation of the EEG. Journal of Psychophysiology, 33. S56. • (9) Pineda, J.A.; Foote, S.L.; Neville, H.J. (1989). "Effects of Locus Coeruleus Lesions on Auditory Event-Related Potentials in Monkey". J. Neurosci 9 (1): 81–93. • (10) Johnson, R.; Jr (1993). "On the neural generators of the P300 component of the event-related potential". Psychophysiology 30 (1): 90–97. PMID 8416066 • (11) Chapman, R.M. & Bragdon, H.R. (1964). Evoked responses to numerical and non-numerical visual stimuli while problem solving. Nature, 203, 1155-1157. • (12) Nieuwenhuis S, Cohen J D. , Aston-Jones G, Decision Making, the P3, and the Locus Coeruleus–Norepinephrine System • (13) P Mobley and P Greengard, 1984, Evidence for widespread effects of noradrenaline on axon terminals in the rat frontal cortex, Yale School of Medicine • (14) Yao WD, Spealman RD, Zhang J, Dopaminergic signaling in dendritic spines, Biochem Pharmacol. 2008 Jun 1;75(11):2055- 69. • (15) Livingstone, Margaret; Ronald Harris-Warrick, Edward Kravitz (1980) "Serotonin and Octopamine Produce Opposite Postures in Lobsters". Science 208 (4439): 76–79. doi:10.1126/science.208.4439.76. PMID 17731572. • (16) Previc FH, 1999, Dopamine and the origins of human intelligence, Flight Stress Protection Division, Brooks Air Force Base, Texas • (17) Morón JA et al., 2002, Dopamine uptake through the norepinephrine transporter in brain regions with low levels of the dopamine transporter: evidence from knock-out mouse lines. The Journal of Neuroscience, January 15, 2002, 22 (2):389–395 • (18) Yavich, Forsberg, Karayiorgou, Gogos, Männistö 2007, Site-Specific Role of Catechol-O-Methyltransferase in. Dopamine Overflow within Prefrontal Cortex and. Dorsal Striatum. Journal of Neuroscience (impact factor: 7.11). 10/2007; 27(38):10196- 209. DOI:10.1523/JNEUROSCI.0665-07.2007
  42. 42. • (19) Derflinger S et al. (2011), Grey-matter atrophy in Alzheimer's disease is asymmetric but not lateralized., J Alzheimers Dis. 2011;25(2):347-57. doi: 10.3233/JAD-2011-110041. • (20) Michael T. Heneka et al., Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine, Proc Natl Acad Sci U S A. 2010 March 30; 107(13): 6058–6063. • (21) Rahul S. Desikan et al., 2010, Selective Disruption of the Cerebral Neocortex in Alzheimer's Disease, the Alzheimer's Disease Neuroimaging Initiative • (22) Cooney, R.E.; et al. (2010). "Neural correlates of rumination in depression". Cognitive Affective and Behavioral Neuroscience 10 (4): 470–478. • (23) M. J. Kempton et al., 2011, Structural Neuroimaging Studies in Major Depressive Disorder, Meta-analysis and Comparison With Bipolar Disorder – Arch Gen Psychiatry. 2011;68(7):675-690. doi:10.1001/archgenpsychiatry.2011.60 • (24) Su B, Wang X, Nunomura A, et al. (December 2008). "Oxidative Stress Signaling in Alzheimer's Disease". Curr Alzheimer Res 5 (6): 525–32. • (25) Magda Ilcewicz-Klimek, Christopher R Honey, Helen S Mayberg (2011-11-18). "A multicenter pilot study of subcallosal cingulate area deep brain stimulation for treatment-resistant depression". Journal of Neurosurgery 116 (2): 315–22. doi:10.3171/2011.10.JNS102122. PMID 22098195 • (26) Aha. Insight experience correlates with solution activation in the right hemisphere EDWARD M. BOWDEN and MARK JUNG-BEQGAAN • (27) Fingelkurts AA, Fingelkurts AA, Rytsälä H, Suominen K, Isometsä E, Kähkönen S, Impaired functional connectivity at EEG alpha and theta frequency bands in major depression, BM-SCIENCE - Brain and Mind Technologies Research Centre, Espoo, Finland. • (28) David Robertson, MD and Emily M Garland , PhD, Dopamine Beta-Hydroxylase Deficiency http://www.ncbi.nlm.nih.gov/books/NBK1474/ • SCIENCE; Indrani,G; 313:1775-1781 (2006) • (28) Lyness S A, Zarow C, Chui H C. Neuron loss in key cholinergic and aminergic nuclei in Alzheimer disease: a meta‐analysis. Neurobiol Aging 2003. 241–23.23 • Cross AJ, Crow TJ, Perry EK, Perry RH, Blessed G, Tomlinson BE., 1981, Reduced dopamine-beta-hydroxylase activity in Alzheimer's disease. • Martinez et al. Dopamine Type 2/3 Receptor Availability in the Striatum and Social Status in Human Volunteers. Biological Psychiatry, 2010; 67 (3): 275 DOI: 10.1016/j.biopsych.2009.07.037 • Petra J J Baarendse et al., Early Social Experience Is Critical for the Development of Cognitive Control and Dopamine Modulation of Prefrontal Cortex Function • Jan P. C. De Bruin et al., Orbital prefrontal cortex, dopamine, and social-agonistic behavior of male long evans rats • http://blogs.scientificamerican.com/primate-diaries/2011/11/17/social-networks-matter/

×