Schzophrenia and Alzheimer's Flashcards

1
Q

Define schizophrenia

A

A psychological disorder characterized by the presence of symptoms that includes delusions, hallucinations, disorganized speech, disorganized behavior, diminished emotional expression, and cognitive impairments.

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2
Q

Name the positive symptoms of schz

A

Delusions and hallucinations (AKA pscyhotic symptoms)

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3
Q

Define delusions

A

misrepresentations of reality

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4
Q

Name and define the 3 types of delusions

A
  • Of grandeur: believing we are someone we are not
    * Of persecution: believing that someone is out to hurt us
    * Paranoid delusions: over suspicious of others in the most non realistic ways (ex: aliens are watching)
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5
Q

Define hallucinations; which type is most common in schz patients?

A

perceptions of sensory events that are not occurring in reality, can involve any of the senses
• Most common in schizophrenia are auditory

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6
Q

Name positive symptoms of schz that are not considered psychotic

A

Disordered speech and behaviours

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7
Q

Define the negative symptoms of schz and their 3 main categories

A

Diminished emotional expressions (AKA flat affect)
• Avolition (reduction in motivations to engage in activities)
• Anhedonia (inability to feel pleasure)
• Alogia (poverty of speech)

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8
Q

Name the 3 main brain abnormalities associated with schz

A
  • Enlargement of brain ventricles (not in all cases, not the cause of the disease)
    * Compresses the close brain regions, which impair their development and leads to symptoms
    • Gray matter loss
      • Temporal, parietal and some part of PFC mostly
    • Lower than normal functioning of prefrontal cortex (Wisconsin Card Sorting Test)
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9
Q

Define the Wisconsin Card Sorting test; how do people with PFC damage do in this task?

A

Asked to sort a deck of cards by shape, color or symbols
• Then the rule changes
• PFC damage: difficulty to switch to a new pattern of sorting

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10
Q

Define the hypofrontality theory of schz

A

idea that activity in the PFC is reduced in people with schizophrenia

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11
Q

Define the dopamine hypothesis of schz

A

idea that a dysfunctional dopaminergic system is at the core of schizophrenia

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12
Q

Define the 1st version of the dopamine hypothesis; what are the problems with this version?

A
  1. Drugs that are effective against schizophrenia block dopamine receptors in the brain
    a. Also, drugs that increase dopamine levels can induce schizophrenic-like symptoms
    b. Problems: does not mention which brain areas affected, does not mention which symptoms affected
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13
Q

Define the 2nd version of the dopamine hypothesis

A
  1. Positive symptoms are due to excessive dopamine neurotransmission in the striatum, and negative due to lack of dopamine neurotransmission in the frontal lobes
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14
Q

Define the 3rd version of the dopamine hypothesis

A
  1. Many factors account for the dysfunction of dopaminergic neurotransmission in schizophrenic patients (therefore to hallucinations)
    a. Those dysfunctions happen in presynaptic neurons and not in D2 receptors
    b. Dopamine dysregulation is linked only to the psychotic symptoms
    c. Excessive dopamine release increases the salience of stimuli to the point where it becomes exaggerated, giving rise to hallucinations
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15
Q

Define the aberrant salience hypothesis

A

c. Excessive dopamine release increases the salience of stimuli to the point where it becomes exaggerated, giving rise to hallucinations

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16
Q

Define the NMDA-receptor-hypofunction hypothesis of schz, name 2 reasons why it might be valid

A

suggests that NMDA receptors are dysfunctional in people w schizophrenia
WHY? ->
• Drugs blocking NMDA receptors induce symptoms similar to schz
• Drugs that increase glutaminergic neurotransmission alleviate these symptoms

17
Q

Name the 4 theories that could explain auditory/verbal hallucinations in schz patients

A

1- Auditory and verbal hallucinations may be due to memories unrelated to present context appearing into consciousness without intention (memories fail to be suppressed by memory system)
• Due to altered connectivity between hippocampus, superior temporal gyrus (auditory cortex), Wernicke’s area, Broca’s area through the striatum - brain areas responsible for language memory and auditory processing
2- Hallucinations may be due to dysfunctioning in self-monitoring
• Perceiving internal speech as externally generated
Due to altered connectivity in frontal areas, anterior cingulate cortex, Broca’s area, and temporal areas (Wernicke’s)
3- Hallucinations due to hyperconnectivity between auditory areas of both hemispheres through corpus callosum
• Source: tinnitus (condition in which sound is perceived with no external stimulation) is due to this
4- Hallucinations may be cause by an alteration in the balance between bottom up sensory processing (perception are influenced by sensory perception) and top down mechanisms (when your perceptions are influenced by your own thoughts)

18
Q

Name the 2 phenomena affected by normal aging in the brain

A

1- Fluid intelligence: ability to think quickly and abstractly. It includes the capacity of working memory and processing speed.
○ Involves processing speed: speed at which info can be analyzed and at which mental tasks are performed
2- Crystallized intelligence: cognitive skills that depend on accumulated wisdom, knowledge, expertise and vocabulary

19
Q

Define Alzheimer’s disease

A

Degenerative brain disease characterized by the severe and progressive loss of memory and other thinking skills to the point where self-care is no longer possible

20
Q

Define the concept of the amyloid-hypothesis of AD

In which parts of the brain does it mainly occur?

A

the hypothesis that AD results from an accumulation of the peptide beta-amyloid, which forms plaques that cause synaptic dysfunction, inflammation, and neuronal death.
• This process is thought to occur mainly in parts of the brain related to memory (enthorinal cortex and hippocampus)

21
Q

Name 2 problems related with the amyloid hypothesis

A
  • Medications developed to reduce amyloid in neurons have not been effective in treating AD
    • The progression of Alzheimer’s disease is more highly related to the effects of other changes than AB plaques formation (ex: inflammation)
22
Q

Explain the 1st step of AD

A

Step 1: mild cognitive impairment
• Short-term memory loss
• Medial Temporal lobe
• 7yrs

23
Q

Explain the 2nd step of AD

A

Step 2: Mild Alzheimer’s
• Reading problems, poor object recognition, poor direction sense
• Lateral/temporal/parietal lobes
2yrs

24
Q

Explain the 3rd step of AD

A

Step 3: Moderate Alzheimer’s
• Poor judgement, impulsivity, short attention
• Frontal lobe
2yrs

25
Q

Explain the 4th step of AD

A

Step 4: Severe Alzheimer’s
• Disease spreads to occipital lobe
• Visual problems
3yrs

26
Q

Define the tau hypothesis of AD

A

Tau Hypothesis of AD: A hypothesis based on the observation that the progression of Alzheimer’s disease is related more to the effects of changes in tau than to the formation of beta-amyloid plaques

27
Q

What is tau?

A

• Tau: microtubule protein

○ Makes the microtubules of the cells collapse and leads to communication problems between neurons

28
Q

Define the metabolism hypothesis of AD

A

hypothesis that AD and type-2 diabetes share common characteristics. People with type-2 diabetes have 1.5 times the risk of developing dementia compared to people without type-2 diabetes