Neuropyrosis: Receptive Quotient and its Role in Alzheimer's Disease

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Receptive Quotient and its role in Alzheimer’s Disease:

Receptive Quotient and its role in Alzheimer’s Disease By Anand Madhu

Alzheimer’s Disease (AD):

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". Human lifespan is up to 120 years, but Alzheimer’s Disease (dementia), cuts it short. Now we’ll explore the cause of Alzheimer’s Disease, which is a mystery to the scientific community.

The DLMS & the NLMS:

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

PowerPoint Presentation:

The brain’s roughly 10 11 neurons are randomly connected by roughly 10 14 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) *

The Dopamine-linked Micro-system :

The Dopamine-linked Micro-system Axon terminal (say)

Dopamine (D) & Norepi (N):

Dopamine (D) & Norepi (N) Dopamine (D) & Norepi (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) The systems within which they act – may be called the Dopamine-linked Micro-system (DLMS) & Norepi-linked Micro-System (NLMS) These Systems 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

The Dopamine-linked Micro-system :

The Dopamine-linked Micro-system Axon terminal (say)

DLMS and NLMS work by boosting Signals:

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 .

Sheffield discovers a new, Axon-centric type of Signalling:

Sheffield discovers a new, Axon-centric type of Signalling Conventional wisdom regarding neuron signalling functionality: Traditionally, it has been known that dendritic spines collect electric signals, and signals add up cumulatively and are relayed further by axons, as shown in the picture on the right. 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 an “ Axonic ” neuron’s axonal elaboration is accompanied by more “ higher order 1 ” dendrital elaboration, as Chatham notes , saying: “The left hemisphere 2 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 Minor correction to be made: I later found out that what I call “higher order” is usually called “lower order”! 2 In the left hemisphere, axonal elaboration is generally lesser, and the opposite trend holds for the right hemisphere (Conventional type flow of information ) Sheffieldian information flow/signal transmission

PowerPoint Presentation:

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

PowerPoint Presentation:

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?

Monoconditional vs. Multiconditional signalling:

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

Monoconditional vs. Multiconditional signalling:

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

Memory – an example of Dopaminic boosting:

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 hyperlink to last viewed Slide ( click only if relevant) Memory 1 Memory 2

Summary: 2 modes of boosting-aided transmission:

(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

Summary – 2: Logic Gates of the CNS:

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

Summary – 3: A package of many parallel circuits:

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)

RQ (Receptive Quotient/Dopaminic Quotient):

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.

Identifying RQ as “behaviors which involve a quantitative dependence on external stimuli”:

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. 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 ). 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! 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. 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

Quantitative ToM:

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 ToM 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

More examples to illustrate the RQ-based lifestyle:

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 ”:-

Are we on the right track?:

Are we on the right track? Relating such kind of quantitative social activity to Dopamine/RQ seems the right thing to do… after all, for example, researchers found that "Fruit flies that are "socially stimulated" have three times the amount of dopamine in their brains than "socially deprived" fruit flies" (SCIENCE; Indrani,G ; 313:1775-1781 (2006)). (Note: We call for qualitative as opposed to such quantitative social activity, rather than the cessation of social activity). Heavily DLMS-involving/quantitative signalling-involving mental activities are: syllogistically-based (thus quantitative*) neuro-calculative lifestyles e.g.: money or stock-chasing, typical corporate matters, ‘cut-throat’ competitionism, “game theory”-based lifestyle etc. * Logically-based lifestyles are, in contrast, qualitative (involving qualitative rather than quantitative signalling), partly since they are optimized thus involve less mental processing.

PowerPoint Presentation:

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

Neuropyrosis (‘overheating of neurons’):

Neuropyrosis (‘overheating of neurons’) The Neuropyrosis theory of Alzheimer’s disease has 3 statements: Dopamine is “alien” in the (upper) brain , an organ that originally was, primarily, the home turf of Octopamine/Norepi ever since the evolution of the brain in the animant (as covered in Paper B , the New Thesis )... The Dopaminergic system is expansionistic in the upper brain It appears that Dopaminergic and Norepic Innervaters “drift”* generally across some areas of the brain, and settle down wherever calculative circuits and/or memories are to be formed. * In mostly quasi-Lamarckian (characteristics acquired during lifetime), but partly Lamarckian ( characteristics passed down to children) and partly Darwinian ( characteristics acquired over generations) manners… An excessively DLMS-based neurostructural ideology, causes overheating, leading to dementia and depression

a.) Dopamine is alien in the upper brain:

a.) Dopamine is alien in the upper brain 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 mostly 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 abnormal *

b.) The Dopaminergic system is expansionistic:

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 ") b.) The Dopaminergic system is expansionistic

a.) Dopamine is alien in the upper brain:

Nearly half the body’s dopamine is outside the brain ( governing linear processes which need only its monoconditional signalling ) – is the design taking a “calculated risk”, in harboring D? 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). The cuckoo characteristic may imply that D is in a quasicalculative (RQ) role thanks to an advanced Norepic substrate. 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 a.), we theorize: problems may arise due to general hyperactivity of Dopamine in the upper brain… as will be discussed in the “Neuropyrosis” theory a.) Dopamine is alien in the upper brain

Alzheimer’s Disease in an overly Dopamine-dependent neurocircuital/structural ideology:

Alzheimer’s Disease in an overly Dopamine-dependent neurocircuital/structural ideology Due to several reasons ( e.g.: the 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 brain generally implies a low level of Norepi and vice versa ……………………………………………….…………..(i) 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 , the source of Norepi, is correlated with levels of N in the brain; hence Alzheimer’s disease is characterized by not just low levels of N, but also, from (i ), an elevated presence of D. In other words an overly DLMS-based neurocircuital ideology, (as in high RQ people), is associated with Alzheimer’s Disease.

PowerPoint Presentation:

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, so that there is more dendrital development (more development of grey matter i.e. mostly dendrites) – suffers damage due to overheating. Why? 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 a brain overly dependent on RQ-type circuits – more DLMSs are required than how many NLMSs are needed in the less-RQ-based brain, because a relatively simplistic (monoconditional) and archaic ( see ch. B here ) logic gate is being overused in the neurocircuital architecture. Thus more number of D-gates are discharging their energies into the net signal volume Since each D/N-LMS activity adds the same amount of energy, that implies an overall greater energy density. Thus a PFC (etc.) that is largely based on DLMSs generally experiences greater signal density.

Confirming the greater signal density in AD:

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, we 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).

Collapse of signal volume in a mostly NLMS-involving architecture vs. increase of signal volume in a mostly DLMS-involving architecture:

Collapse of signal volume in a mostly NLMS-involving architecture vs. increase of signal volume in a mostly DLMS-involving architecture This is an indicative idea about how signal volume progressively reduces in a Norepic milieu. In contrast, signal volume often progressively increases , in a Dopaminic milieu.

The Neuropyrosis Theory of AD:

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 neuron, 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:

PowerPoint Presentation:

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).

Depression:

Depression Dementia is bad by itself. But what is worse about the neuropyrosis process, is that those who suffer Alzheimer's disease – also seem to suffer depression. 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 ). ” This proves that depression is linked to a DLMSs-majority state of brain circuits. In the neuropyrosis-suffering brain, t he overall process doesn’t involve qualitative areas (like the NLT-area ), and therefore quantitatively burdens 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.

––––– References–––––– :

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