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Summary Neuropsychology of Ageing and Dementia 2025 - A LOT OF PRACTICE QUESTIONS - Lecture and Literature-Based Questions

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This practice exam contains many questions about the literature and lectures. In addition, you will receive many examples that help you understand complex models. This document will prepare you for the exam!












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Documentinformatie

Geüpload op
13 januari 2025
Bestand laatst geupdate op
11 februari 2025
Aantal pagina's
34
Geschreven in
2024/2025
Type
Samenvatting

Voorbeeld van de inhoud

Practice exam: Neuropsychology of ageing and dementia
Questions with a line are very important!

Questions
Lecture 1: Basics of Aging
1a. Population Decline: Does population decline occur only in more developed countries, or
does it also happen eventually in less developed countries?
1b. Chronological Age: What is chronological age?
1c. Biological Age: Define biological age.
1d. Functional Age: What is functional age?
1e. Psychological Age: Define psychological age.
1f. Social Age: What is social age?
1g. Types of Aging: What is the difference between normative aging, successful aging, and
positive aging?
1h. Primary vs. Secondary Aging: What distinguishes primary aging from secondary aging?
2a. Selective Optimization with Compensation Model (SOC): Explain the SOC model of
aging, focusing on the components of selection, optimization, and compensation.
2b. Ecological Model of Aging: Explain the ecological model of aging and how the
interaction between competence and the environment influences adaptation.
3a. Morbidity: What does morbidity mean?
3b. Mortality: What does mortality mean?
4a. Programmed Theories: Define programmed theories and indicate if they relate to
primary or secondary aging.
4b. Stochastic Theories: Define stochastic theories and indicate if they relate to primary or
secondary aging.
4c. Theory Differences: What is the primary distinction between programmed theories and
stochastic theories?
4d. Programmed Theory Types: Name all programmed theories.
4e. Explanation of Programmed Theories: Explain each programmed theory.
4f. Stochastic Theory Types: Name all stochastic theories.
4g. Explanation of Stochastic Theories: Explain each stochastic theory.
5a. Stress: what are the two systems that are involved in a stress response?
5b. Stress: stress triggers a physiological activation that results in the secretion of stress-
related hormones, how are these hormones called?
5c. Stress: What happens when somebody is prolonged exposed to these hormones (name 2).
5d. Stress: in which organism does the stress system quickly return to normal levels?
Lecture 2:
6a. What does FMRI stand for?
6b. What does PET stand for?
6c. What is a disadvantage of a PET?
6d. Where does the radioactive bind itself to?
7a. Which part of the brain starts to lose weight at young adults?
7b. Which brain regions reduce in volume with age, name four?
7c. Which brain regions stay stable or with minimal reduction with age, name 2?
7d. Which brain region shows the steepest rate of atrophy?
7e. Which brain regions shows the second steepest rate of atrophy?
8a. What is white matter? And where can the greatest loses be found in aging? And what does
this explain?

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,8b. Does cerebrospinal fluid increase or decrease when people age, explain your answer.
8c. What does anterior and posterior mean?
8d. Explain the anterior-posterior gradient.
8e. When you get older do controlled processes like cooking, booking a vacation faster,
slower or remains the same?
8f. Ageing gives a decline in 4 cognitive abilities, which abilities are these?
9a. Which two patterns are there in age-related functioning? Explain both.
9b. One of them is paradoxal, explain what makes it paradoxal.
9c. The one that is not paradoxal, explain why this age-related functioning exist.
9d. Explain the theory of scaffolding and the two key factors.
10a. Name the five theories of cognitive aging.
10b. Explain each of the theories. With Core idea’s and key points.
11a. What is osteoporosis and atherosclerosis?

Lecture 3: Mild cognitive impairment
1a. What are the 4 different possible causations of MCI?
1b. What is the pathology of Alzheimer disease. Fill in the blanks. Plaque formation begins
with abnormal misfolding of beta-amyloid protein which leads to neurofibrillary-tangles, the
consequence of this is = synaptic-disruption and neurodegeneration.
1c. To continue 1b, the memory impairments are (in Alzheimer) because of the degeneration
of the hippocampus and the entorhinal cortex.

Lecture 4: Vascular Dementia & Frontotemporal
Dementia
1a. What is this:




1b. What is this:




1c. What is this:




1d. What is an ischemic stroke?
1e. What is a hemorrhagic stroke?
1f. When somebody has a large vessel stroke the effects are relatively focal. With a small
vessel stroke the effects are relatively diffuse.

2

,1g. Which one is more often associated with vascular dementia?
1h. What is the clinical manifestation when an artery is suffering from lesions?
Choices: Prosopagnosia, Alexia with or without agraphia, Hemiplegia, Personality changes,
Homonymous hemianopia, Abulia, Visual agnosia, Aphasia, Paraplegia, Hemianesthesia,
Balint syndrome, Executive dysfunctions
Middle cerebral artery: (3)
Hemiplegia
Aphasia
Hemianesthesia
Anterior cerebral artery: (4)
Paraplegia
Abulia
Executive dysfunctions
Personality changes
Posterior cerebral artery: (5)
Homonymous hemianopia
Alexia with or without agraphia
Visual agnosia/
Balint syndrome
Prosopagnosia
1i. Are people with Alzheimer’s or vascular dementia more depressed? And why is that?
1j. What is the hereditary disease that causes vascular dementia?
1k. What causes FTD?
1l. In FTD you can find hypometabolism in the medial-prefrontal-cortex and lateral-
prefrontal-cortex.
1m. Name al the FTD variants.
1n. In BV-FTD what are the symptoms when the following brain regions are disturbed?
Which symptom is de most severe?
Choices: [Disinhibition or distractibility], Decreased agreeableness, Antisocial behavior, Poor
impulse control, Apathy, Stereotyped behavior, Akinetic mutism, [Dramatic changes in
beliefs, attitude and/or religious sentiment], Progressive non-fluent aphasia
 Orbitofrontal lobe (5)
 Anterior cingulate cortex and Medial frontal lobe (1)
 Predominately right hemisphere (1)
 Left frontal cortex (late stage)
 Anterior cingulate cortex and Medial frontal (late stage)
1o. When FTD progresses, you get features of Klüver-Bucy syndrome. What kind of
symptoms does this give?
1r. What is FTD – primary progressive aphasia?
1s. What is semantic dementia and what will it lead to? (2)
1t. What is non-fluent primary progressive aphasia? (2) & (4 problems area’s)
1u. Logopenic primary progressive, what is it? (4)
1v. What is the difference between sematic, logopenic and non-fluent aphasia variant.
1u. What are the risk factors for vascular dementia?

Lecture 5: PDD, LWD, HD
1a. What are Lewy body diseases and what are Lewy body dementias?
1b. In Lewy body disease we have Neuronal-inclusions of the proteins: ubiquitin and alpha-
synuclein. These are found subcortically in the substantia-nigra and in Alzheimer it’s
cortically. In Alzheimer’s the protein is different, it’s the amyloid-beta protein.

3

, 2a. Parkinson’s disease is caused by the death of dopaminergic neurons in the substance nigra.
2b. In Parkinson’s disease, the dopamine levels are affected. Because of this there is not
enough dopamine, this causes mmovement-ddisorders. The cells of the substantia nigra
degenerate which gives the consequences of the decreased amount of dopamine. This then
results in the dysfunction of the striatum and the areas connected to the striatum.
2c. Which impairment in cognition do people with Parkinson disease have and which one is
the biggest and why? (5)
2cc. Which impairments in neurocognition do people with Parkinson disease have? Name 5
and which one is a precursor for dementia?
2d. In Parkinson, cortical disorders such as aphasia, apraxia, agnosia are not common, but in
Alzheimer it is. People with Parkinson disease dementia have impairment in retrieving
information … memory, but the recognition is intact. In tests they can recognize figures with
a bit of help in Alzheimer this is not the case since they cannot store new information
anymore.
2e. What is the difference between dementia with Lewy bodies and Parkinson’s disease
dementia?
3a. Which impairments in cognition do people with Lewy body have? (3)
3b. Which clock is made by somebody with Lewy body dementia, and which one is made by
one that has Alzheimer’s?




3c. Name 3 core features of dementia with Lewy body and 2 suggestive features.
3d. Fill in the table




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There are a lot of practice questions, they are very difficult though. I did pass my course and the practice questions helped a lot.

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