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PSYCH 3410 > Lecture 9 - Brain Damage and Neuroplasticity > Flashcards

Lecture 9 - Brain Damage and Neuroplasticity Flashcards

1
Q

How many people does Huntington’s Disease affect?

A

A rare disease affecting about 1:10,000 people

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2
Q

What is Huntington’s Disease?

A

Progressive motor disorder of middle age and older adults with a strong genetic basis

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3
Q

What is Huntington’s disease caused by?

A

A single dominant gene mutation (Huntingtin gene –> Huntingtin protein)

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4
Q

What does Huntington’s Disease cause?

A

Starts with fidgetiness and jerkiness and then progresses into severe loss of motor control and dementia

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5
Q

What do you find in a Huntington patients brain?

A

Clumps of proteins

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6
Q

What are the new insights of Huntington’s?

A

HTT gene accumulates CAG repeats that do not get fixed by DNA repair mechanisms

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7
Q

What do the number of CAG repeats correlate to?

A

The symptom severity

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8
Q

What does over 150+ CAG repeats cause?

A

Dysfunction in cellular regulation which leads to apoptosis

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9
Q

How can Hungtinton’s Disease be tested?

A

By doing a blood test to look for CAG repeats - can be detected 20 years prior before symptoms start

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10
Q

What does Huntington’s Disease cause?

A

A neurodegenerative disorder that causes the gradual breakdown of the basal ganglia, a group of nerve cells in the brain that control movement.

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11
Q

Why do Huntington’s patients seem to have larger ventricles?

A

The disease causes significant atrophy (shrinkage) of brain tissue, particularly in the striatum region, which leads to an expansion of the fluid-filled spaces called ventricles within the brain;

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12
Q

What is the Striatum?

A

The striatum is a cluster of interconnected nuclei that form a part of the basal ganglia. It is involved in decision making functions, such as motor control, emotion, habit formation, and reward.

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13
Q

What is Multiple Sclerosis?

A

Progressive loss of CNA myelin (oligodendrocytes)

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14
Q

What is Multiple Sclerosis believe to be caused by?

A

Autoimmune condition

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15
Q

Because multiple sclerosis happens in the CNS, what can’t happen?

A

Any regeneration (remyelination)

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16
Q

What does Multiple Sclerosis lead to?

A

Neuronal degeneration (signals aren’t flowing as efficiently)

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17
Q

What is the typical onset of Multiple Sclerosis?

A

Early adulthood –> progressive

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18
Q

What are some advanced symptoms of multiple sclerosis?

A

Muscle weakness, numbness, tremor, visual distrubances, lack of motor control

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19
Q

What is common with multiple sclerosis?

A

Periods of remission

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20
Q

What drugs have been used for MS?

A

Immunomodulators may slow the progression or symptoms

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21
Q

What is the genetic predisposition for MS?

A

25% concordance in twins

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22
Q

What gender has a higher chance of getting at?

A

3 times higher in females than males

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23
Q

What are the chances in white people of European descent?

A

0.15% greater incidence

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24
Q

What are the genes associated with MS?

A

Several genes in the immune system and non-coding RNAs

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25
What are some environmental factors of MS?
if you grew up in a colder climate, may be more likely to get MS Viral or Bacterial Infections (Epstein-Barr virus) Lifestyle Factors (diet, smoking, exercise)
26
What are epigenetic factors for MS?
Lack of Vitamin D
27
What is the Location Factors involved in MS?
Higher latitudes (less sun exposure)
28
What are the treatments for MS?
Corticosteroids (reduce inflammation), disease modifying treatment (immunomoduators), Physical Therapy
29
What is some ongoing research treatments?
Stem cell therapies, lipid regulation, and biotin (vitamin B7)
30
What is the Experimental Autoimmune Encephalomyelitis Model of MS?
"Experimental Autoimmune Encephalomyelitis (EAE)" refers to a laboratory animal model widely used to study multiple sclerosis (MS), essentially mimicking the key features of the disease in humans, including inflammation, demyelination, and axonal damage within the central nervous system
31
What is Active EAE?
Immunize with CNS antigens (myelin or myelin proteins) to stimulate immune response in mouse (causes the mouses immune system to attack itself)
32
What is passive EAE?
The transfer of autoimmune (T cells) to naive animals
33
What is Spontaneous EAE?
Transgenic mouse models
34
What is a Transgenic Mouse Model?
A laboratory mouse that has been genetically engineered to have DNA from another source inserted into its genome, allowing researchers to study specific gene functions or model human diseases
35
What is the EAE good for?
Developing some treatment for MOGAD
36
What is EAE limited to?
T4 mediated autoimmune processes
37
What is Alzheimers disease the most common cause of?
Dementia
38
What is Alzheimers related to?
Age related (10% over 65, 35% over 85)
39
What is uncommon with Alzheimers
Early onset (age 40) but common with individuals who have down syndrome
40
Who is Alzheimers more prevalent in?
Females (hormonal changes)
41
What do we see with an Alzheimers autopsy?
Tay tangles, amyloid plaques and loss of neurons and potentially micro bleeds
42
What are the stages of Alzheimers progression?
Preclincial Phase Prodomal Phase Dementia Stage
43
What is the Preclinical Phase?
Some neuropathology is present in the brain, but no behavioural or cognitive systems
44
What is the Prodromal Phase?
Mild cognitive impairment (confusion, selective memory and attention loss)
45
What is the Dementia Stage?
Memory and attention deficits, personality changes, confusion, anxiety, speech deficits, neurological impairment
46
What are the Tau Tangles we see in Alzheimers?
- Inside the cell (inside neurons) - Tau protein holds together microtubules - Phoshorylated Tau clump together instead
47
What are Amyloid Plaques?
Clumps of protein that build up in the brain, especially in the gray matter
48
How are Amyloid Plaques formed?
Amyloid Precursor Protein (APP) is cleaved incorrectly and forms amyloid-B
49
What happens in a diseased neuron?
Tangled clumps of Tau protein and the microtubules start to fall apart
50
What enzymes cleaves an amyloid precursor protein?
a-secretase
51
What do APP mutations increase?
B-secreate cleavage
52
What happens when the amyloid is cleaved incorrectly?
Excess amyloid accumulation
53
Where in the brain is there age highest number of plaques?
Amygdala, Hippocampus, prefrontal cortex and parietal cortex
54
What matter is Alzheimers a disease of?
The grey matter
55
What has early onset Alzheimers been linked to genetically?
4 specific genes for amyloid or its regulators
56
What are the genes for early onset?
Presenilin proteins 1, 2 and APP on chromosome 21
57
What are the genes for later onset?
15+ genes for amyloid or tau Ex: apolipoprotein (APOE4) --> 50% of Alzheimers
58
What is the Pathogenic Spread Hypothesis?
The proximity (closer) a neuron is to the amyloid may cause altered response to simulation
59
What is there a decline in for Alzheimers?
Acetylcholine (ACh)
60
What could you prescribe a Alzheimers patients?
Ach agonists (so acetyl choline can stay in the synapse for longer periods of time)
61
What could Immunotherapy for Alzheimers patients do?
Produce antibodies against the amyloid proteins so your immune system can increase the breakdown of amyloid-B
62
Who develops amyloid plaques?
Only humans and a few other primates
63
What is Transgenic?
An animal that has the genes of another species
64
What did they do to mice to test Alzheimers?
Introduced amyloid plaques and noticed that the plaques caused the same symptoms in mice as AD, also put Tau into mice and saw similar Ad symptoms
65
At the UofG, what did they notice with transgenic mice?
At the age of 9 months they had no long term memory

PSYCH 3410 (18 decks)

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