A Computational Cognitive Model of the Brain

Author(s):  
Zhiwei Shi ◽  
Hong Hu ◽  
Zhongzhi Shi

Recent fruitful progresses on brain science have largely broadened our understanding of the cerebrum. These great works led us to propose a computational cognitive model based on a graphical model that we carried out before. The model possesses many attractive properties, including distinctive knowledge representation, the capability of knowledge accumulation, active (top-down) attention, subjective similarity measurement, and attention-guided disambiguation. It also has “consciousness” and can even “think” and “make inference.” To some extent, it works just like the human brain does. The experimental evidence demonstrates that it can give reasonable computational explanation on the human phenomenon of forgetting. Although there are still some undetermined details and neurobiological mechanisms deserving consideration, our work presents a meaningful attempt to give further insights into the brain’s functions.

Author(s):  
Alba J. Jerónimo ◽  
María P. Barrera ◽  
Manuel F. Caro ◽  
Adán A. Gómez

A cognitive model is a computational model of internal information processing mechanisms of the brain for the purposes of comprehension and prediction. CARINA metacognitive architecture runs cognitive models. However, CARINA does not currently have mechanisms to store and learn from cognitive models executed in the past. Semantic knowledge representation is a field of study which concentrates on using formal symbols to a collection of propositions, objects, object properties, and relations among objects. In CARINA Beliefs are a form of represent the semantic knowledge. The aim of this chapter is to formally describe a CARINA-based cognitive model through of denotational mathematics and to represent these models using a technique of semantic knowledge representation called beliefs. All the knowledge received by CARINA is stored in the semantic memory in the form of beliefs. Thus, a cognitive model represented through beliefs will be ready to be stored in semantic memory of the metacognitive architecture CARINA. Finally, an illustrative example is presented.


2006 ◽  
Vol 4 (13) ◽  
pp. 193-206 ◽  
Author(s):  
Steve Furber ◽  
Steve Temple

The quest to build an electronic computer based on the operational principles of biological brains has attracted attention over many years. The hope is that, by emulating the brain, it will be possible to capture some of its capabilities and thereby bridge the very large gulf that separates mankind from machines. At present, however, knowledge about the operational principles of the brain is far from complete, so attempts at emulation must employ a great deal of assumption and guesswork to fill the gaps in the experimental evidence. The sheer scale and complexity of the human brain still defies attempts to model it in its entirety at the neuronal level, but Moore's Law is closing this gap and machines with the potential to emulate the brain (so far as we can estimate the computing power required) are no more than a decade or so away. Do computer engineers have something to contribute, alongside neuroscientists, psychologists, mathematicians and others, to the understanding of brain and mind, which remains as one of the great frontiers of science?


Author(s):  
Preecha Yupapin ◽  
Amiri I. S. ◽  
Ali J. ◽  
Ponsuwancharoen N. ◽  
Youplao P.

The sequence of the human brain can be configured by the originated strongly coupling fields to a pair of the ionic substances(bio-cells) within the microtubules. From which the dipole oscillation begins and transports by the strong trapped force, which is known as a tweezer. The tweezers are the trapped polaritons, which are the electrical charges with information. They will be collected on the brain surface and transport via the liquid core guide wave, which is the mixture of blood content and water. The oscillation frequency is called the Rabi frequency, is formed by the two-level atom system. Our aim will manipulate the Rabi oscillation by an on-chip device, where the quantum outputs may help to form the realistic human brain function for humanoid robotic applications.


Author(s):  
Sally M. Essawy ◽  
Basil Kamel ◽  
Mohamed S. Elsawy

Some buildings hold certain qualities of space design similar to those originated from nature in harmony with its surroundings. These buildings, mostly associated with religious beliefs and practices, allow for human comfort and a unique state of mind. This paper aims to verify such effect on the human brain. It concentrates on measuring brain waves when the user is located in several spots (coordinates) in some of these buildings. Several experiments are conducted on selected case studies to identify whether certain buildings affect the brain wave frequencies of their users or not. These are measured in terms of Brain Wave Frequency Charts through EEG Device. The changes identified on the brain were then translated into a brain diagram that reflects the spiritual experience all through the trip inside the selected buildings. This could then be used in architecture to enhance such unique quality.


2019 ◽  
Author(s):  
Chris Robert Harrison Brown

Attention has long been characterised within prominent models as reflecting a competition between goal-driven and stimulus-driven processes. It remains unclear, however, how involuntary attentional capture by affective stimuli, such as threat-laden content, fits into such models. While such effects were traditionally held to reflect stimulus-driven processes, recent research has increasingly implicated a critical role of goal-driven processes. Here we test an alternative goal-driven account of involuntary attentional capture by threat, using an experimental manipulation of goal-driven attention. To this end we combined the classic ‘contingent capture’ and ‘emotion-induced blink’ (EIB) paradigms in an RSVP task with both positive or threatening target search goals. Across six experiments, positive and threat distractors were presented in peripheral, parafoveal, and central locations. Across all distractor locations, we found that involuntary attentional capture by irrelevant threatening distractors could be induced via the adoption of a search goal for a threatening category; adopting a goal for a positive category conversely led to capture only by positive stimuli. Our findings provide direct experimental evidence for a causal role of voluntary goals in involuntary capture by irrelevant threat stimuli, and hence demonstrate the plausibility of a top-down account of this phenomenon. We discuss the implications of these findings in relation to current cognitive models of attention and clinical disorders.


Author(s):  
Henrik Hogh-Olesen

Chapter 7 takes the investigation of the aesthetic impulse into the human brain to understand, first, why only we—and not our closest relatives among the primates—express ourselves aesthetically; and second, how the brain reacts when presented with aesthetic material. Brain scans are less useful when you are interested in the Why of aesthetic behavior rather than the How. Nevertheless, some brain studies have been ground-breaking, and neuroaesthetics offers a pivotal argument for the key function of the aesthetic impulse in human lives; it shows us that the brain’s reward circuit is activated when we are presented with aesthetic objects and stimuli. For why reward a perception or an activity that is evolutionarily useless and worthless in relation to human existence?


2021 ◽  
Vol 16 ◽  
pp. 263310552110187
Author(s):  
Christopher D Link

Numerous studies have identified microbial sequences or epitopes in pathological and non-pathological human brain samples. It has not been resolved if these observations are artifactual, or truly represent population of the brain by microbes. Given the tempting speculation that resident microbes could play a role in the many neuropsychiatric and neurodegenerative diseases that currently lack clear etiologies, there is a strong motivation to determine the “ground truth” of microbial existence in living brains. Here I argue that the evidence for the presence of microbes in diseased brains is quite strong, but a compelling demonstration of resident microbes in the healthy human brain remains to be done. Dedicated animal models studies may be required to determine if there is indeed a “brain microbiome.”


2020 ◽  
Vol 31 (8) ◽  
pp. 803-816
Author(s):  
Umberto di Porzio

AbstractThe environment increased complexity required more neural functions to develop in the hominin brains, and the hominins adapted to the complexity by developing a bigger brain with a greater interconnection between its parts. Thus, complex environments drove the growth of the brain. In about two million years during hominin evolution, the brain increased three folds in size, one of the largest and most complex amongst mammals, relative to body size. The size increase has led to anatomical reorganization and complex neuronal interactions in a relatively small skull. At birth, the human brain is only about 20% of its adult size. That facilitates the passage through the birth canal. Therefore, the human brain, especially cortex, develops postnatally in a rich stimulating environment with continuous brain wiring and rewiring and insertion of billions of new neurons. One of the consequence is that in the newborn brain, neuroplasticity is always turned “on” and it remains active throughout life, which gave humans the ability to adapt to complex and often hostile environments, integrate external experiences, solve problems, elaborate abstract ideas and innovative technologies, store a lot of information. Besides, hominins acquired unique abilities as music, language, and intense social cooperation. Overwhelming ecological, social, and cultural challenges have made the human brain so unique. From these events, as well as the molecular genetic changes that took place in those million years, under the pressure of natural selection, derive the distinctive cognitive abilities that have led us to complex social organizations and made our species successful.


2021 ◽  
Vol 22 (15) ◽  
pp. 8325
Author(s):  
Paola Zanfardino ◽  
Stefano Doccini ◽  
Filippo M. Santorelli ◽  
Vittoria Petruzzella

Oxidative phosphorylation (OxPhos) is the basic function of mitochondria, although the landscape of mitochondrial functions is continuously growing to include more aspects of cellular homeostasis. Thanks to the application of -omics technologies to the study of the OxPhos system, novel features emerge from the cataloging of novel proteins as mitochondrial thus adding details to the mitochondrial proteome and defining novel metabolic cellular interrelations, especially in the human brain. We focussed on the diversity of bioenergetics demand and different aspects of mitochondrial structure, functions, and dysfunction in the brain. Definition such as ‘mitoexome’, ‘mitoproteome’ and ‘mitointeractome’ have entered the field of ‘mitochondrial medicine’. In this context, we reviewed several genetic defects that hamper the last step of aerobic metabolism, mostly involving the nervous tissue as one of the most prominent energy-dependent tissues and, as consequence, as a primary target of mitochondrial dysfunction. The dual genetic origin of the OxPhos complexes is one of the reasons for the complexity of the genotype-phenotype correlation when facing human diseases associated with mitochondrial defects. Such complexity clinically manifests with extremely heterogeneous symptoms, ranging from organ-specific to multisystemic dysfunction with different clinical courses. Finally, we briefly discuss the future directions of the multi-omics study of human brain disorders.


mBio ◽  
2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Felipe H. Santiago-Tirado ◽  
Michael D. Onken ◽  
John A. Cooper ◽  
Robyn S. Klein ◽  
Tamara L. Doering

ABSTRACT The blood-brain barrier (BBB) protects the central nervous system (CNS) by restricting the passage of molecules and microorganisms. Despite this barrier, however, the fungal pathogen Cryptococcus neoformans invades the brain, causing a meningoencephalitis that is estimated to kill over 600,000 people annually. Cryptococcal infection begins in the lung, and experimental evidence suggests that host phagocytes play a role in subsequent dissemination, although this role remains ill defined. Additionally, the disparate experimental approaches that have been used to probe various potential routes of BBB transit make it impossible to assess their relative contributions, confounding any integrated understanding of cryptococcal brain entry. Here we used an in vitro model BBB to show that a “Trojan horse” mechanism contributes significantly to fungal barrier crossing and that host factors regulate this process independently of free fungal transit. We also, for the first time, directly imaged C. neoformans-containing phagocytes crossing the BBB, showing that they do so via transendothelial pores. Finally, we found that Trojan horse crossing enables CNS entry of fungal mutants that cannot otherwise traverse the BBB, and we demonstrate additional intercellular interactions that may contribute to brain entry. Our work elucidates the mechanism of cryptococcal brain invasion and offers approaches to study other neuropathogens. IMPORTANCE The fungal pathogen Cryptococcus neoformans invades the brain, causing a meningoencephalitis that kills hundreds of thousands of people each year. One route that has been proposed for this brain entry is a Trojan horse mechanism, whereby the fungus crosses the blood-brain barrier (BBB) as a passenger inside host phagocytes. Although indirect experimental evidence supports this intriguing mechanism, it has never been directly visualized. Here we directly image Trojan horse transit and show that it is regulated independently of free fungal entry, contributes to cryptococcal BBB crossing, and allows mutant fungi that cannot enter alone to invade the brain. IMPORTANCE The fungal pathogen Cryptococcus neoformans invades the brain, causing a meningoencephalitis that kills hundreds of thousands of people each year. One route that has been proposed for this brain entry is a Trojan horse mechanism, whereby the fungus crosses the blood-brain barrier (BBB) as a passenger inside host phagocytes. Although indirect experimental evidence supports this intriguing mechanism, it has never been directly visualized. Here we directly image Trojan horse transit and show that it is regulated independently of free fungal entry, contributes to cryptococcal BBB crossing, and allows mutant fungi that cannot enter alone to invade the brain.


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