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

1. Neuropyrosis
Receptive Quotient and its
role in Alzheimer’s Disease
By Anand Madhu (Droog)

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. 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. 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. The DLMS & the NLMS
Seeing the Dopamine-Linked and
Norepi-Linked Micro-Systems as the
Logic Gates of the Nervous System

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. 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. 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. 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. 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. 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. Monoconditional signalling Multiconditional signalling
DLMS/Dopamine’s NLMS/Norepi’s
How do the DLMS and the NLMS work?

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. 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. 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. 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. (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. 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. • 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. 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. 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. • 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. 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. 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. • 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. 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. 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. 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. • “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. 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. • 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.  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. 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. 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. • 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. 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. 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. 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. 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. 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

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