NEUROSCIENCE RESEARCH ADVANCES -- CONTENTS -- PREFACE -- BEHAVIORS OF PHOSPHORYLATED MICROTUBULESASSOCIATEDPROTEIN TAU (TAU) - A ROLE INNEURONAL AND GLIAL APOPTOSIS, WHITE MATTERLESION, TOPOGRAPHICAL ACCENTUATION AND14-3-3 PROTEIN EXPRESSION IN OFNEUROFIBRILLARY TANGLES OF ALZHEIMER'SDISEASE AND OTHER TAUOPATHIES -- ABSTRACT -- INTRODUCTION -- DISCOVERY OF ALZHEIMER'S NFT STAGEINGAND OF NEUROPIL THREADS -- DISCOVERY OF PRETANGLES, EVIDENCE OF EVOLUTIONARYSTAGES FOR NFT AND MODIFICATION OF EXTRACELLULARGHOST TANGLES -- HOW IS TAU PHOSPHORYLATED? -- IMMUNOHISTOCHEMISTRY OF NFT IN RELATION WITHDIFFERENT PHOSPHORYLATION SITES -- MATERIALS AND METHODS -- NFT SHOW TOPOGRAPHICAL ACCENTUATION ACCORDINGTO DIFFERENT PHOSPHORYLATION SITES -- RELATIONSHIP OF THREE NFT CONFIGURATIONS TOPHOSPHORYLATION SITES. HOW DO THE PHOSPHORYLATION SITESOF TAU CONTRIBUTE TO DIFFERENCE IN TANGLE CONFIGURATIONAMONG PRE-NFT, INT-NFT AND EXT-NFT? -- THREE-REPEAT (3R) AND FOUR-REPEAT (4R) TAUOPATHIES -- EXTRACELLULAR GHOST TANGLES ARE 3R, PRETANGLES AREPRESUMED TO BE 4R AND INTRACELLULAR TANGLES ARE HYBRIDOF 3R AND 4R. AT8 IS NOT A IMMUNOLABELING MARKER FORPRE-NFT AND PRE-NFT ARE 4R TAU AND POSITIVE FORPSER422 IN ALZHEIMER'S DISEASE -- NFT AND NEURONAL APOPTOSIS -- 14-3-3 PROTEINS AND NFT -- WHITE MATTER CHANGES AND SUBCORTICAL ALZHEIMERDEGENERATION. FILLING BODIES ARE LYSOSOMES -- GLIAL APOPTOSIS IS ASSOCIATED WITH BAP -- FAMILIAL AD AND UNUSUAL ACCENTUATION OF NFTIN THE HIPPOCAMPAL SUBDIVISIONS -- FRONTOTEMPORAL DEMENTIA AND PARKINSONISM LINKEDTO CHROMOSOME 17, PSP AND CBD -- REFERENCES -- BRAIN DEVELOPMENT AND NEURODEVELOPMENTALOUTCOME IN INFANTS WITH CONGENITAL HEARTDISEASE -- ABSTRACT -- INTRODUCTION -- 1. NEURODEVELOPMENTAL OUTCOMES OF INFANTS WITH CHD -- 1.1. Clinical and Radiographic Evidence of Impaired Pre-OperativeNeurological Status.

1.2. Short-Term Neurological Outcome after Surgery -- 1.3. Neurodevelopmental Outcomes for Survivors at School Age and Beyond -- 1.3.1. Neurodevelopmental outcomes in children with single ventricles -- 1.3.2. Neurodevelopmental outcomes in children with transposition of the great arteries -- 1.4. Quality of Life -- 2. RISK FACTORS FOR ADVERSE NEURODEVELOPMENTAL OUTCOME -- 2.1. Preoperative Neurological Status -- 2.1.1. Intrauterine factors that impact cerebral blood flow and neurodevelopment -- 2.1.2. Congenital brain and developmental abnormalities -- 2.1.3. Acquired preoperative brain injury -- 2.2. Intraoperative Factors that Impact Neurodevelopmental Outcome -- 2.2.1. Acid-base strategies -- 2.2.2. Hemodilution during bypass -- 2.2.3. Circulatory arrest versus low flow bypass -- 2.3 Post-operative Factors that Impact Neurodevelopmental Outcome -- 3. NEUROMONITORING AND NEUROPROTECTIVE STRATEGIES -- 3.1. Peri and Intraoperative Neuroprotective Strategies -- 3.2 Neuromonitoring Techniques -- 3.2.1. Transcranial doppler (TCD) -- 3.2.2. Continuous electroencephalography -- 3.2.3. Near infrared spectroscopy (NIRS) -- 2.2.4. Multi-modal neuromonitoring -- CONCLUSIONS -- ACKNOWLEDGMENT -- REFERENCES -- THE DISTINCT ROLE OF PIN1 IN THE DEVELOPMENTAND TREATMENT OF NEURODEGENERATIVETAUOPATHIES -- ABSTRACT -- 1. INTRODUCTION -- 2. TAU PHOSPHORYLATION AT THR231 -- 3. POST-PHOSPHORYLATIONAL REGULATION OF TAU BY PIN1 -- 3.1. Pin1 Binds to and Isomerizes the pThr231-Pro Motif in Tau -- 3.2. Pin1 Restores Phosphorylated Tau Function -- 3.3. Pin1 Prevents Phosphorylated Tau Accumulation -- 4. PROTECTIVE IMPACT OF PIN1 ON WILD-TYPE TAU-INDUCEDTAUOPATHY IN MICE AND AD -- 5. AGGRAVATING IMPACT OF PIN1 ON P301L TAU-INDUCEDTAUOPATHY IN MICE -- 6. CONCLUSION -- REFERENCES -- A NOVEL APPROACH TO MEMORYNEUROMODULATION USING MUSIC:A LITERATURE REVIEW -- ABSTRACT.

1. EMOTIONAL AROUSAL AND MEMORY -- 1.1. Underlying Mechanisms -- 1.1.1. The role of noradrenergic modulation -- 1.1.2. Amygdala mediation -- 1.2. Hyperconsolidation of Emotional Stimuli -- 1.3. Moderating Factors -- 2. A NOVEL APPROACH TO MEMORY NEUROMODULATION: MUSIC -- 2.1. Music and Emotion -- 2.2. Music and Cognitive Performance -- 3. CONCLUSION -- REFERENCES -- ELECTROENCEPHALOGRAPHY, AMPLITUDEINTEGRATEDELECTROENCEPHALOGRAPHYAND NEURODEVELOPMENTAL OUTCOME INPREMATURE INFANTS -- ABSTRACT -- INTRODUCTION -- 1.0. DEFINITIONS AND BASIC PRINCIPLES OF EEG/AEEG -- 1.1 General EEG Principles -- 1.2. General aEEG Principles -- 1.3. Use and Limitations of EEG/aEEG in the NICU -- 2.0. MATURATIONAL CHANGES IN EEG/AEEG -- 2.1. EEG Maturation in Preterm Infants -- 2.1.1. Interburst intervals (IBI) -- 2.1.2. Periods of continuous EEG activity -- 2.1.3. Synchrony -- 2.1.4. Reactivity -- 2.1.5. EEG waveform patterns[7] -- 2.1.6. Sleep-wake cycling (SWC) -- 2.2. aEEG Maturation in Preterm Infants -- 3.0. EEG/AEEG ABNORMALITIES AND PREDICTION OFNEURODEVELOPMENTAL OUTCOME -- 3.1. Prognostic Value of EEG in Premature Infants -- 3.1.1. Abnormal waveforms -- 3.1.2. Classification systems for EEG abnormalities in preterm infants -- 3.2. Prognostic Value of aEEG in Premature Infants -- CONCLUSION -- REFERENCES -- TANGLE DOMINANT DEMENTIA -- ABSTRACT -- INTRODUCTION -- Major Clinical Features of TDD -- General Neuropathology of TDD -- MATERIAL AND METHODS -- RESULTS -- Comparison of Clinical Features -- Comparison of Neuropathologic Features -- Synopsis -- CONCLUSION -- NOTE ADDED IN PROOF -- REFERENCES -- DOES EXPOSURE TO METHYLPHENIDATEDURING ADOLESCENT AFFECT THE RESPONSETO METHYLPHENIDATE IN ADULTHOOD? -- ABSTRACT -- INTRODUCTION -- MATERIALS AND METHODS -- Subjects -- Open field apparatus -- Wheel - running apparatus -- Drug -- Experimental Protocol -- Analysis.

Results -- Saline control -- Acute phase - comparing ED2 to ED-1 -- (A) Open Field Assay: -- (B) Running Wheel Assay: -- Induction phase - comparing ED-7 to ED-2 -- (A) Open Field Assay: -- (B) Running Wheel Assay: -- Expression phase - comparing ED-11 to ED-2 -- (A) Open Field Assay: -- (B) Running Wheel Assay -- DISCUSSION -- REFERENCES -- THE SPATIAL PATTERNS OF TAU IMMUNOPOSITIVENEURONAL CYTOPLASMIC INCLUSIONS (NCI)IN THE TAUOPATHIES -- ABSTRACT -- INTRODUCTION -- THE TAUOPATHIES -- Alzheimer's Disease -- Pick's Disease -- Corticobasal Degeneration -- Progressive Supranuclear Palsy -- MATERIALS AND METHODS -- Cases -- Tissue Preparation -- Morphometric Methods -- Data Analysis -- SPATIAL PATTERNS EXHIBITED BY THE TAU POSITIVE NCI -- CONCLUSION -- ACKNOWLEDGMENTS -- REFERENCES -- CAMP AND NEURODEVELOPMENT -- ABSTRACT -- 1. THE CYCLIC AMP PATHWAYS -- 1.1. The Protein Kinase A -- 1.2. The Exchange Proteins Activated by cAMP -- 1.3. The Cyclic AMP & Calcium Pathways -- 1.4. The Cyclic AMP-Response Element-Binding Protein Activation -- 2. RELATIONSHIP BETWEEN RECEPTORS ONTOGENESIS, CAMPLEVELS AND NEURODEVELOPMENT MODULATION -- 2.1. Adenosine Receptors Family -- 2.2. Dopamine Receptors Family -- 2.3. Glutamate Receptors Family -- 2.4. Gamma Aminobutyric Acid Receptors Family -- 2.5. Peptide Pituitary Adenylate Cyclase - Activating Polypeptide ReceptorsFamily -- 2.6. Acetylcholine Receptors Family -- 2.7. Melatonin Receptors Family -- 3. FURTHER THAN TRANSCRIPTIONS FACTORS -- 4. CONCLUSION -- REFERENCES -- EPILEPSY AND PHYSICAL EXERCISE:HUMAN AND ANIMAL STUDIES -- ABSTRACT -- INTRODUCTION -- 1. Overview of Epilepsy -- 2. Epilepsy and Exercise: Human's Studies -- 2.1. Risks of sports participation -- 2.3. Epilepsy and exercise physiology -- 3. Epilepsy and Exercise: Animals' Studies -- 3.1. Animal models of epilepsy -- 3.1.1. Kindling model.

3.1.2. Pilocarpine model -- 3.2. Effect of physical exercise in experimental models of epilepsy -- CONCLUSION -- ACKNOWLEDGMENTS -- REFERENCES -- UNDERSTANDING SCHIZOPHRENIA PATHOGENESISFROM DEVELOPMENTAL ORIGINS OF HEALTHAND DISEASE (DOHAD) -- ABSTRACT -- REFERENCES -- INDEX.