Midterm

Question 1

Which brain regions enlarged in the London Taxi driver study?

Answer 1

1. Medial prefrontal cortex (tracking distance to destination)
2. Right lateral prefrontal cortex (seeing unexpected features, eg blocked off road)
3. Anterior prefrontal cortex (Spontaneous route planning - eg if need to make a diversion)
4. Hippocampus (initial route planning)
5. Rostral splenial cortex (seeing expected landmarks, streets and desinations)

Question 2

What are the neurological implications of the Nun Study?

Answer 2

1. Increased brain reserve is resulted from more complex language capacity and higher education level.
2. This may have to with redundant neural networks for functional tasks.

Question 3

What are the neurocognitive and neuroanatomical implications of MCI and interventions for it?

Answer 3

Individuals diagnosed with it have significant cognitive impairments in multiple domains, including memory, language, attention, and executive function.

Correspondingly, they have significant reductions in gray matter volume in the medial temporal, prefrontal, and parietal cortices.

Cognitive interventions have been proven to improve both of these domains.

Question 4

What is cognitive reserves?

Answer 4

Cognitive reserve refers to the brain’s capacity to develop new neural pathways to blunt the impacts of Alzheimer’s.

Question 5

What is brain reserve?

Answer 5

Brain reserve refers to the brain’s capacity to endure physical injury. This deals with brain size, synaptic density, and connectivity.

Question 6

What is the trajectory of schizophrenia?

Answer 6

1. The prodromal phase is the earliest phase of the illness, characterized by subtle changes in behavior and cognition, such as social withdrawal, decreased motivation, and impaired attention. They are difficulty to distinguish from normal adolescent behavior or other psychological illnesses.
2. The active phase of schizophrenia is characterized by the presence of positive symptoms, such as delusions, hallucinations, and disorganized speech or behavior. These symptoms may wax and wane over time and can be severe enough to impair daily functioning.
3. The residual phase of schizophrenia is the final phase of the illness, characterized by the presence of negative symptoms, such as apathy, social withdrawal, and decreased motivation. These symptoms may persist even after the active phase has subsided and can significantly impair functioning and quality of life.

Question 7

What is the trajectory of Alzheimer’s?

Answer 7

1. Preclinical: individuals may have biochemical or pathological evidence of Alzheimer’s disease, but they do not yet show any clinical symptoms.
2. Mild Cognitive Impairment: individuals may begin to experience memory loss, difficulty with language, trouble with problem-solving or planning, and decreased attention or concentration, but they are still able to perform everyday activities.
3. Mild Dementia Due to Alzheimer’s Disease: During this stage, individuals begin to experience more significant cognitive impairments that interfere with daily activities. These impairments may include memory loss, difficulty with language, difficulty with problem-solving or planning, decreased attention or concentration, and changes in mood or behavior.
4. Moderate Dementia Due to Alzheimer’s Disease: In this stage, individuals experience more severe cognitive impairments that require assistance with daily activities. These impairments may include difficulty with communication, wandering or getting lost, difficulty with toileting, and changes in mood or behavior.
5. Severe Dementia Due to Alzheimer’s Disease: During this stage, individuals require full-time assistance with all activities of daily living. They may experience difficulty with swallowing, lose the ability to speak, and become bedridden.

Question 8

What is the prevalence of schizophrenia?

Answer 8

1. Roughly at 1%.
2. Does not seem to have a strong genetic component.
3. Specific to humans.
4. Persistent across our verbal history.

Question 9

What is the prevalence of Alzheimer’s disease?

Answer 9

It is the most common cause of dementia, accounting for 60-80% of all cases.

It is estimated the global prevalence of Alzheimer’s disease to be 27 million in 2018, with projections suggesting that this number will increase to 106 million by 2050.

Question 10

What neurocognitive deficits are found in Alzheimer’s disease?

Answer 10

gradual loss of cognitive function, including memory, language, decision-making abilities, as well as changes in behavior and personality.

Question 11

What are the potential treatments for schizophrenia?

Answer 11

While antipsychotic medications are the first-line treatment for schizophrenia and have been shown to be effective in reducing symptom severity and improving functioning, there are still several potential treatments that could be explored. Cognitive-behavioral therapy and family therapy, may also be beneficial in reducing symptom severity and improving functioning.

Question 12

What are the potential treatments for Alzheimer’s?

Answer 12

Medication and cognitive therapy designed to improve cognition and memory.

Related cognitive therapies:

Psychosocial interventions:

1. Cognitive stimulation therapy involves engaging individuals with Alzheimer’s disease in structured activities that are designed to improve cognitive function and social interaction.
2. Reality orientation therapy involves providing individuals with Alzheimer’s disease with information about their surroundings, such as the time of day and location.
3. Reminiscence therapy involves encouraging individuals with Alzheimer’s disease to recall past events and experiences, which can help to improve their mood and cognitive function.

Question 13

What was Kandel’s methodology in studying the Aplysia?

Answer 13

By applying electrical shock to the tail of the animal at the same time as tactile stimulation of the siphon, an amplified withdrawal response (of both the gill and siphon) is produced. This new behavior lasts up to an hour. Repeated application of this allows Kandel and his team to study the transition of memory storage from short-term to long-term.

Question 14

What neurological implications did Kandel’s work on Aplysia have?

Answer 14

Kandel recorded the activity of individual neurons in the Aplysia nervous system to show that experience can modify the strength of synaptic connections between neurons.

Specifically, repeated pairing of sensory input with a tail shock led to the activation of the PKA pathway, which in turn led to changes in gene expression and protein synthesis that were necessary for the formation of long-term memory. These changes include the synthesis of new proteins and the modification of existing proteins, such as ion channels and receptors, which are involved in the strengthening of synaptic connections between neurons.

Question 15

What implications did Kandel’s work have on neuropsychological disorders?

Answer 15

Alzheimer’s disease is a disorder characterized by memory deficits, and Barnes et al. (2017) found that the activation of the cAMP-dependent protein kinase (PKA) pathway was reduced in the brains of individuals with Alzheimer’s disease.

Which means cognitive training/therapy program can align their trajectories with dopamine’s activating actions on PKA. This also means attention must play a key role in such programs.

Question 16

In Kandel’s work, how is implicit short-term memory produced?

Answer 16

In the Aplysia:
1. stimulation to the tail activates serotonin in an interneuron.
2. The serotonin activates cyclic adenosine monophosphate (cAMP) in the sensory neuron directly triggered by the stimulus.
3. cAMP in turn activates cAMP-dependent protein kinase, which amplifies depolarization strength.
4. This lasts for hours.

Question 17

In Kandel’s work, how is short-term memory translated into long-term memory in the Aplysia?

Answer 17

1. Spaced repetitious applications of the stimulus.
2. In addition to serotonin’s activation of cAMP and PKA, mitogen-activated protein kinase is also activated.
3. Both PKA and MAPK moves into the cell nucleus and begins a transcription process.
4. This cascade is initiated by cAMP response element binding protein 1 (CREB-1) which leads to the protein synthesis of new synapses.
5. This synaptic construction process is buffered by the actions of CREB-2, which opposes/regulates that of CREB-1.
6. A time-dependent regression process is managed by cell adhesion molecules (CAM), a substance that induces retraction of new synapses.

Question 18

In Kandel’s work, how is LTP in the hippocampus different from long-term memory storage of implicit memory?

Answer 18

That the process is initiated by dopamine (instead of serotonin), and with it attention is required.

Question 19

In Kandel’s work, what happens to newly formed synapses in LTP without attention?

Answer 19

They retract in a matter of hours.