This thesis is concerned with the computational modelling and simulation of physiological structures and cognitive functions of brains through the use of artificial neural nets. While the structures of these models are loosely related to neurons and physiological structures observed in brains, the extent to which we can accept claims about how neurons and brains really function based on such models depends largely on judgments about the fitness of (virtual) computer experiments as empirical evidence. The thesis examines the computational foundations of neural models, neural nets, and some computational models of higher cognitive functions in terms of their ability to provide empirical support for theories within the framework of Parallel Distributed Processing (PDP). Models of higher cognitive functions in this framework are often presented in forms that hybridise top-down (e.g. employing terminology from Psychology or Linguistics) and bottom-up (neurons and neural circuits) approaches to cognition. In this thesis I argue that the use of terminology from either approach can blind us to the highly theory-laden nature of the models, and that this tends to produce overly optimistic evaluations of the empirical value of computer experiments on these models. I argue, further, that some classes of computational models and simulations based on methodologies that hybridise top-down and bottom-up approaches are ill-designed. Consequently, many of the theoretical claims based on these models cannot be supported by experiments with such models. As a result, I question the effectiveness of computer experiments with artificial neural nets as an empirical technique for cognitive modelling.

Despite considerable evidence in older populations that food intake can improve mental performance, little is known about the acute effects of feeding on cognition in the newborn period, a time when learning and memory are critical for discovering and adapting to everyday experiences. Feeding occurs well over 2500 times in the first year of life, raising the possibility that iterative effects on cognition may have cumulative effects over time. We recently demonstrated feeding enhancement of memory in two-to-three day old infants. Infants tested after a feed (versus before) displayed better memory for unfamiliar spoken words they previously habituated to and that were represented after a 100s delay. In this Doctoral Thesis, Studies 1 and 2 explore further the influence of feeding on short-term retention of spoken words. Memory was assessed using headturning and the Habituation-Recovery response. Study 1 extended the effect to older infants aged two-to-three weeks. Memory was enhanced after a feed over even longer delays, including 100s, 200s, 300s, 400s, and 500s. The overall gain in memory as measured by prefeed and postfeed differences at each delay was over two minutes long. Because newborn infants are more likely to hear recurrent words spoken by familiar voices, auditory experiences that they preferentially recognize, Study 2 looked at the separate effects of familiarity and feeding. Two day-old infants were assessed for either familiar speech-sound ("baby" spoken by the mother) or unfamiliar speech-sound from Study 1 ("beagle" spoken by a female stranger). The baby-mother sound stimulus was remembered better over a retention interval of 85 seconds than unfamiliar beagle-stranger, suggesting a strong influence of familiarity. To define the extent of the feeding effect, Study 3 examined sensorimotor processing of a reflex response. Three day-olds were assessed on habituation and retention of habituation of the glabella blink reflex over delays of 8s and l8s. No effect of feeding was found. Taken together, the implications of these findings are twofold. First, enhancement of memory for speech-sound by iterative feeding or recurrent exposure to familiar speech-sound stimuli may facilitate the acquisition of language. Second, feeding effects on cognition may depend on the nature of the task and previous experience with the stimulus. Further research is necessary for identifying what kinds of information and what processing abilities are more susceptible to the effects of feeding in early infancy.

This thesis investigates the hypothesis that emotions play an influential role in cognition. Interference between facial emotional expression processing and selected tasks is measured using a variety of experimental methods. Prior to the main experimental chapters, the collection and assessment (Chapter 2, Exp. 1) of stimulus materials is described. Experiments 2-11 then concentrate on the likelihood of interference with other types of information from the face. Findings using a Garner design suggest that, although identity processing may be independent of expression variation, expression processing may be influenced by variation in identity (Exps. 2-4). Continued use of this design with sex (Exps. 6-7) and gaze direction (Exps. 9-10) information appears to support the (mutual) independence of these facial dimensions from expression. This is, however, in contrast to studies that indicate the modification of masculinity judgements by expression (Exp. 5), and the interaction of gaze direction and expression when participants rate how interesting they find a face (Exp. 8). Further to this, a search task (Exp. 11) shows that slower responses to an angry (cf. happy) face looking at us, may be due to the presence of an aversive mouth. Experiments 12-15 test for interference in the field of time perception: complex interactions between expression and encoder and decoder sex are indicated. Finally, Experiments 16-17 find that exposure to a sequence in which the majority of faces are angry depresses probability learning, and that prior exposure to varying quantities of angry and happy faces affects our later memory for them. Overall, there is evidence that exposure to emotional expressions may affect other (selected)c ognitive processesd ependingu pon which expressionsa re used and which experimental methods are chosen. It is suggested that future investigations would benefit from techniques that describe the temporal profile of an emotional response.

This thesis is concerned with the computational modelling and simulation of physiological structures and cognitive functions of brains through the use of artificial neural nets. While the structures of these models are loosely related to neurons and physiological structures observed in brains, the extent to which we can accept claims about how neurons and brains really function based on such models depends largely on judgments about the fitness of (virtual) computer experiments as empirical evidence. The thesis examines the computational foundations of neural models, neural nets, and some computational models of higher cognitive functions in terms of their ability to provide empirical support for theories within the framework of Parallel Distributed Processing (PDP). Models of higher cognitive functions in this framework are often presented in forms that hybridise top-down (e.g. employing terminology from Psychology or Linguistics) and bottom-up (neurons and neural circuits) approaches to cognition. In this thesis I argue that the use of terminology from either approach can blind us to the highly theory-laden nature of the models, and that this tends to produce overly optimistic evaluations of the empirical value of computer experiments on these models. I argue, further, that some classes of computational models and simulations based on methodologies that hybridise top-down and bottom-up approaches are ill-designed. Consequently, many of the theoretical claims based on these models cannot be supported by experiments with such models. As a result, I question the effectiveness of computer experiments with artificial neural nets as an empirical technique for cognitive modelling.

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by Mei Chun Cheung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 34-41). / Abstract and questionare in English and Chinese. / ABSTRACT --- p.ii / ACKNOWLEDGEMENTS --- p.iii / TABLE OF CONTENTS --- p.iv / LIST OF TABLES --- p.v / Chapter CHAPTER I - --- INTRODUCTION --- p.1 / Chapter CHAPTER II - --- METHOD --- p.7 / Chapter CHAPTER III - --- RESULTS --- p.17 / Chapter CHAPTER IV - --- DISCUSSION --- p.29 / REFERENCES --- p.34 / APPENDIX --- p.42

No description available.

Alzheimer's disease (AD) is the most common form of dementia. As the prevalence of AD increases with age, population aging will inevitably lead to an exponential increase in the proportion of older persons suffering from this disease. According to 2005 WHO estimate, 26.6 million people (approximately 0.55% of the general population) suffered from this disease. AD not only affects intellectual and functional abilities, it is also associated with significant neuropsychiatric disturbances. The pathogenesis of AD is characterized by widespread cerebral atrophy, abnormal deposition of amyloid plaques and tau protein in the central nervous system. While the classical histopathological features of AD are well recognized, exact physiological mechanisms that initiate the cascade of neural degeneration are still under active investigation. / As mentioned, the telomere length studies focused on ethically Chinese subjects recruited from two independent samples. The first clinical sample consisted of 411 older people and the other sample from healthy aging study, 976 community dwelling men were recruited. All subjects were assessed with the Cantonese version of the Mini-mental State Examination (CMMSE) for global cognitive function. Genomic DNA of the subjects was extracted from the peripheral whole blood sample. Lengths of the telomere were measured with Quantitative Real-Time PCR and the Ct ratio of the telomere and a control gene (36B4) of each sample was compared with the standard curve constructed with 4 selected sample's telomere lengths measured previously by Southern blotting. / For the first association study of the cell cycle checkpoint genes and AD, sample was recruited from a prospective study of cognitive function and risk factors for development of AD. 701 elderly were clinically evaluated for diagnosis of AD by psychiatrists. For this sample, genotyping of tagging SNPs of the 10 cell-cycle checkpoint genes were carried out by Restriction Fragment Length Polymorphism (RFLP) analysis. All tagging SNPs were selected from HapMap database and 5000bp upstream and downstream regions of each gene was also included. / For the results, the association study with cell cycle checkpoint genes, there was no SNPs found to be associated with diagnosis of clinical AD. We also found out that telomere length was associated with age in both two healthy aging men and clinical samples. There was no association between education and telomere lengths. For subjects in the healthy aging study, participants with CMMSE scores fell into the lowest 25% were found to have shorter telomere lengths. Similar result was found in the clinical AD sample. / In the study, telomere lengths were negatively associated with age. As the telomere will be shortened for each cell cycle, this finding correlated with physiological function at a cellular level. Statistical analysis also showed that shorter telomere lengths were found in subjects with poorer cognitive function. However, as age is a major determinant for cognitive impairments, further studies are recommended to evaluate the interaction effects of age in this association. Telomere shortening will cause cell senescence, and may be associated with faster neuronal degeneration, thus affecting cognitive function. Further studies should be conducted to examine its usefulness as an adjuvant biomarker for risk stratification of AD intervention trials. / Recent researches begin to unfold the physiological significance of telomere. A telomere is a repetitive region at the end of a chromosome. Basic functions of telomeres are involved with protection of the chromosome during replication and preventing chromosomal rearrangement or fusion. Abnormal telomere lengthening may be related to cancerous conditions. At a cellular level, telomere may also be related to aging and limitation in cell lifespan. In my study, I aimed to evaluate the association between the lengths of telomere and global cognitive function in community dwelling Chinese older persons in Hong Kong. As the length of telomere is also determined by the turnover rates of cells, apart from association study of telomere lengths and cognitive function, I also tried to study the association of genes related to cell cycles and AD. Polymorphisms of ten cell-cycle checkpoint genes, i.e. RB1, CDKN1A, CDK5R1, CDK2AP1, CDKN2A, CDKN2C, MDM2, P53, GSK3B, TPND1 and CDKN1B genes, were chosen in my project. / The thesis comprised of three studies. The first study was an association study of cell cycle checkpoint gene single nucleotide polymorphisms (SNPs) with clinical diagnosis of AD. The second study was an association study of telomere lengths and clinical diagnosis of AD in a clinical sample of patients suffering from the disease. The third study was an association study of the telomere lengths and global cognitive status in a group of active community dwelling older men who participated in a healthy aging study. / Lau, San Shing. / Adviser: Linda C.W. Lam. / Source: Dissertation Abstracts International, Volume: 73-01, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 101-124). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.