Pay close attention to all lectures and actively engage with the material for effective exam review. This includes taking thorough notes and revisiting key concepts regularly.
For students with accommodations, it’s important to stay after class to discuss any necessary arrangements to ensure a fair testing environment.
Understanding gene-environment interactions is crucial as they significantly affect individual behavior and cognitive development. These interactions can determine susceptibility to various psychological disorders.
Discussions often center around favorable interactions that may enhance development and unfavorable interactions that could lead to risks or diseases.
The aging brain undergoes various changes, including a reduction in brain volume and alterations in neuronal connectivity. It’s important to understand that brain development continues well beyond early childhood, with significant changes throughout adolescence and into adulthood.
One critical aspect of aging is neuronal death, known as apoptosis, which leads to the loss of synaptic contacts essential for effective communication between neurons.
Synaptogenesis: This refers to the formation of synapses between neurons during early development, which sets the foundation for brain functionality.
Apoptosis: As part of normal brain development, certain neural cells will die off, resulting in the loss of some initial synaptic contacts.
Synaptic Rearrangement: Following the pruning of synapses, remaining synapses reorganize and strengthen, a process that continues throughout adulthood and is shaped by experiences and intellectual stimulation.
Pruning: A critical phase occurs during the pre-teen years where significant neuron contact loss is observed, particularly in the frontal cortex, essential for higher-order thinking and decision-making.
Adolescence is marked by hormonal changes and brain restructuring, which can lead to behavioral changes, including increased risk-taking behaviors due to ongoing brain development.
An examination of synaptic activity reveals patterns of pruning and stability from ages 5 to 20, covering both childhood and adolescence. These changes reflect the evolving demands of cognitive and social functioning.
Physical changes in the brain, including structural reorganization, are normal aspects of development that continue to influence cognition into adulthood.
Fragile X Syndrome: This genetic disorder is characterized by an impairment in synapse retention, often leading to intellectual disabilities and distinct physical traits such as a long face and large ears. The disorder arises from mutations in the FMR1 gene located on the X chromosome, disrupting proteins crucial for synaptic pruning.
Differences also exist in how genetic disorders affect males and females, with varying prevalence and manifestations of inherited conditions.
Genotype: Refers to the genetic makeup that can predispose individuals to specific disorders, emphasizing the biological underpinnings of mental health.
Phenylketonuria (PKU): A genetic disorder caused by the absence of the enzyme phenylalanine hydroxylase, resulting in the buildup of phenylalanine which can lead to severe intellectual disability if not managed. Early diagnosis and adherence to a special diet low in phenylalanine are critical for preventing brain damage and promoting healthy development.
Physical Changes: As the brain ages, it often experiences atrophy, particularly in the hippocampus, the area crucial for memory and learning. Despite these changes, elderly brains maintain essential metabolic functions, requiring glucose and oxygen supply.
Cerebral Metabolism: Normal aging can see stable cerebral metabolism, while cognitive decline associated with diseases such as Alzheimer’s presents markedly different neurological challenges.
A progressive neurodegenerative disorder characterized by memory loss, confusion, and a decline in cognitive function primarily impacting older adults. Understanding the distinction between normal aging and Alzheimer’s is key, with Alzheimer’s displaying more profound memory deficits and cortical dysfunctions.
Pathophysiology: The disease is linked to the degeneration of acetylcholine-producing neurons and the accumulation of amyloid plaques in the brain, disrupting normal neuronal communication.
Available treatment strategies, such as cholinesterase inhibitors, aim to prolong the activity of acetylcholine in the brain, potentially mitigating some symptoms.
Encouraging continued mental engagement and socialization for older adults may help delay cognitive decline and improve overall quality of life.
Recommendations include participation in activities that promote both physical exercise and mental stimulation, such as puzzles, social interactions, and lifelong learning pursuits, which are crucial for maintaining brain health as one ages.