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Integrative Understanding of Emergent Brain Properties, Quantum Brain Hypotheses, and Connectome Alterations in Dementia are Key Challenges to Conquer Alzheimer's Disease.

Kuljiš RO - Front Neurol (2010)

Bottom Line: The biological substrate for cognition remains a challenge as much as defining this function of living beings.Here, we examine some of the difficulties to understand normal and disordered cognition in humans.These unresolved dilemmas include critically the as yet untested quantum brain hypothesis, and the embryonic attempts to develop and define the so-called connectome in humans and in non-human models of disease.

View Article: PubMed Central - PubMed

Affiliation: The Brain-Mind Project, Inc, Encephalogistics, Inc, University of Miami Miami, FL, USA.

ABSTRACT
The biological substrate for cognition remains a challenge as much as defining this function of living beings. Here, we examine some of the difficulties to understand normal and disordered cognition in humans. We use aspects of Alzheimer's disease and related disorders to illustrate how the wealth of information at many conceptually separate, even intellectually decoupled, physical scales - in particular at the Molecular Neuroscience versus Systems Neuroscience/Neuropsychology levels - presents a challenge in terms of true interdisciplinary integration towards a coherent understanding. These unresolved dilemmas include critically the as yet untested quantum brain hypothesis, and the embryonic attempts to develop and define the so-called connectome in humans and in non-human models of disease. To mitigate these challenges, we propose a scheme incorporating the vast array of scales of the space and time (space-time) manifold from at least the subatomic through cognitive-behavioral dimensions of inquiry, to achieve a new understanding of both normal and disordered cognition, that is essential for a new era of progress in the Generative Sciences and its application to translational efforts for disease prevention and treatment.

No MeSH data available.


Related in: MedlinePlus

Schematic diagram of the selective laminar distribution of senile plaques and neurofibrillary tangles in various regions of the cortex and the pulvinar nucleus of the thalamus, a structure highly interconnected with a vast array of so-called association cortices targeted heavily and early by sporadic Alzheimer's disease (sAD). This view of the pathobiology of AD focuses on the circuitry affected and is limited to the resolution of the light microscopy. Thus, while it helps to understand the connections that are affected and to establish their correlation with the clinical manifestations of the disorder, it does not convey information about the ultrastructural, electrophysiological, functional imaging, and molecular domains, among others.
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Figure 2: Schematic diagram of the selective laminar distribution of senile plaques and neurofibrillary tangles in various regions of the cortex and the pulvinar nucleus of the thalamus, a structure highly interconnected with a vast array of so-called association cortices targeted heavily and early by sporadic Alzheimer's disease (sAD). This view of the pathobiology of AD focuses on the circuitry affected and is limited to the resolution of the light microscopy. Thus, while it helps to understand the connections that are affected and to establish their correlation with the clinical manifestations of the disorder, it does not convey information about the ultrastructural, electrophysiological, functional imaging, and molecular domains, among others.

Mentions: In fact, in sporadic AD, quick and merely cursory inspection of most regions of the cerebral cortex appears to indicate a seemingly extensive, random involvement. However, a slightly closer examination armed both with a familiarity with the microscopic anatomy of this region, and methodology to reveal aspects of its regional, areal, laminar, cellular, and supra-cellular assembly (a.k.a. modular) organization reveals that the involvement – although spread among many functionally different regions – is remarkably selective both in space and in time throughout the cerebral cortex (Kuljiš, 1994, 1997; Kuljiš and Tikoo, 1997). This region-, area-, layer- cell-, and cortical module component-selective targeting (Figures 2 and 3) defies to this day even the most highly imaginative molecular hypotheses of the etiology and pathogenesis of the condition, since virtually all such approaches are forced to treat the brain as a “black box” (e.g., Figure 4) essentially ignoring even basic elements of its anatomical and functional organization that have been known in some instances since the 19th Century (Kuljiš, 1997, 2009b). Thus, since they ignore key aspects of brain organization and function, strictly molecular explanations of neurodegenerative disorders may be condemned to remain incomplete (e.g., Fernández et al., 2008; Figure 4), but may succeed in a small number of cases – due to fortuitously useful oversimplification – in being applied to effective treatment and prevention (Kuljiš, 2009a, 2010).


Integrative Understanding of Emergent Brain Properties, Quantum Brain Hypotheses, and Connectome Alterations in Dementia are Key Challenges to Conquer Alzheimer's Disease.

Kuljiš RO - Front Neurol (2010)

Schematic diagram of the selective laminar distribution of senile plaques and neurofibrillary tangles in various regions of the cortex and the pulvinar nucleus of the thalamus, a structure highly interconnected with a vast array of so-called association cortices targeted heavily and early by sporadic Alzheimer's disease (sAD). This view of the pathobiology of AD focuses on the circuitry affected and is limited to the resolution of the light microscopy. Thus, while it helps to understand the connections that are affected and to establish their correlation with the clinical manifestations of the disorder, it does not convey information about the ultrastructural, electrophysiological, functional imaging, and molecular domains, among others.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3008926&req=5

Figure 2: Schematic diagram of the selective laminar distribution of senile plaques and neurofibrillary tangles in various regions of the cortex and the pulvinar nucleus of the thalamus, a structure highly interconnected with a vast array of so-called association cortices targeted heavily and early by sporadic Alzheimer's disease (sAD). This view of the pathobiology of AD focuses on the circuitry affected and is limited to the resolution of the light microscopy. Thus, while it helps to understand the connections that are affected and to establish their correlation with the clinical manifestations of the disorder, it does not convey information about the ultrastructural, electrophysiological, functional imaging, and molecular domains, among others.
Mentions: In fact, in sporadic AD, quick and merely cursory inspection of most regions of the cerebral cortex appears to indicate a seemingly extensive, random involvement. However, a slightly closer examination armed both with a familiarity with the microscopic anatomy of this region, and methodology to reveal aspects of its regional, areal, laminar, cellular, and supra-cellular assembly (a.k.a. modular) organization reveals that the involvement – although spread among many functionally different regions – is remarkably selective both in space and in time throughout the cerebral cortex (Kuljiš, 1994, 1997; Kuljiš and Tikoo, 1997). This region-, area-, layer- cell-, and cortical module component-selective targeting (Figures 2 and 3) defies to this day even the most highly imaginative molecular hypotheses of the etiology and pathogenesis of the condition, since virtually all such approaches are forced to treat the brain as a “black box” (e.g., Figure 4) essentially ignoring even basic elements of its anatomical and functional organization that have been known in some instances since the 19th Century (Kuljiš, 1997, 2009b). Thus, since they ignore key aspects of brain organization and function, strictly molecular explanations of neurodegenerative disorders may be condemned to remain incomplete (e.g., Fernández et al., 2008; Figure 4), but may succeed in a small number of cases – due to fortuitously useful oversimplification – in being applied to effective treatment and prevention (Kuljiš, 2009a, 2010).

Bottom Line: The biological substrate for cognition remains a challenge as much as defining this function of living beings.Here, we examine some of the difficulties to understand normal and disordered cognition in humans.These unresolved dilemmas include critically the as yet untested quantum brain hypothesis, and the embryonic attempts to develop and define the so-called connectome in humans and in non-human models of disease.

View Article: PubMed Central - PubMed

Affiliation: The Brain-Mind Project, Inc, Encephalogistics, Inc, University of Miami Miami, FL, USA.

ABSTRACT
The biological substrate for cognition remains a challenge as much as defining this function of living beings. Here, we examine some of the difficulties to understand normal and disordered cognition in humans. We use aspects of Alzheimer's disease and related disorders to illustrate how the wealth of information at many conceptually separate, even intellectually decoupled, physical scales - in particular at the Molecular Neuroscience versus Systems Neuroscience/Neuropsychology levels - presents a challenge in terms of true interdisciplinary integration towards a coherent understanding. These unresolved dilemmas include critically the as yet untested quantum brain hypothesis, and the embryonic attempts to develop and define the so-called connectome in humans and in non-human models of disease. To mitigate these challenges, we propose a scheme incorporating the vast array of scales of the space and time (space-time) manifold from at least the subatomic through cognitive-behavioral dimensions of inquiry, to achieve a new understanding of both normal and disordered cognition, that is essential for a new era of progress in the Generative Sciences and its application to translational efforts for disease prevention and treatment.

No MeSH data available.


Related in: MedlinePlus