Lecture 18 - Alzheimer's Disease Flashcards

1
Q

Is Dementia a disease?

A

No. Dementia is a symptom, characterised by memory loss and impaired cognition and behaviour, caused by various disorders/diseases, such as Alzheimer’s disease.

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2
Q

What is the most common cause of Dementia?

A

Alzheimer’s disease.

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3
Q

What is the genetic risk factor associated with Alzheimer’s disease?

A

Carriage of a variant of the APOE gene.

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4
Q

Is Alzheimer’s disease considered a polygenic disease?

A

Yes.

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5
Q

There is an inheritable form of Alzheimer’s disease. How is this version of the disease different to the acquired/non-inherited form and is it common?

A

No. The inherited version of AD is not common.
This version of AD involves the over production of amyloid proteins in the brain, as opposed to the acquired version of AD, which involves a decline in the ability to remove amyloid proteins from the brain.

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6
Q

What is the amyloid hypothesis?

A

The amyloid hypothesis posits that AD is caused by the production of beta amyloid segments that join together and form a plaque which attaches to neurons and eventually leads to neuronal death.

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7
Q

To date, official diagnosis of AD is only possible postmortem.
What are some new ways that AD can be potentially diagnosed in the living?

A

Special types of PET scan can be used to detect beta-amyloid in the brain.

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8
Q

What are other ways that AD can be tested for, or tests that can be done to determine risk factors for AD?

A

Measure amyloid levels in Cerebral Spinal Fluid.
Blood tests.

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9
Q

What is TAU and what is it’s relationship/association with AD?

A

Tau is a protein that stabilises microtiubules in axons. Tau can be phosphorylated at many different regions and hyperphosphorylation of tau prevents it from stabilising microtubles. Hyperphosphorylation also leads to the tau to aggregate together and form NEUROFIBRILLARY TANGLES, which are a key biomarker for AD.
These tangles impair the function and signalling abilities of neurons.

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10
Q

What are tauopathies?

A

Tauopathies are diseases associated with neurofibrillary tangles of tau proteins.
AD is one of these diseases, characterised by aggregates of neurofibrillary tangles in the medial temporal lobes - hence the characteristic dementia associated with AD.

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11
Q

What is meant when AD is referred to as an amyloid mediated tauopathy?

A

It is hypothesised that the beta amyloid plaques someone cause tau to misbehave/hyperphosphorylate, which leads to the production of neurofibrillary tangles. Neurons then detect that something is wrong and self-destruct. This releases these tau aggregates into the extracellular space. It is then thought that these tau aggregates “infect” other neurons and the process repeats itself, in turn leading to neuronal/cortex deterioration.

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12
Q

What are some ways that tau aggregates can be detected?

A

PET scans.
CSF measuring.
Blood tests under development.

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13
Q

We have a 19 year window to intervene and attempt to prevent the development of AD, from the time that “at risk” levels of biomarkers can be detected.
Who did this research?

A

This research was done by Jo Robertson and her research team Villemagne et al.

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14
Q

AD does not necessarily kill patient’s, but does lead to cognitive and behavioural impairments that can lead to death.
True?

A

True.

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15
Q

Dementia is a key diagnostic criteria for….?

A

AD

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16
Q

What are some diagnostic criteria for AD?

A

Dementia.
Clear history of cognitive decline.
Exclusion of other potential causes of these symptoms.

17
Q

What are some behavioural and cognitive symptoms in AD?

A

Memory impairments.
Navigation/orientation impairments.
Language impairment.

18
Q

How is dementia diagnosed?

A

Need to measure DECLINE in cognition.
Dementia is diagnosed when there is impairment to everyday function.
Cognitive tasks are used to diagnose dementia.

19
Q

What are some of the treatment options for AD?

A

Anti-amyloid antibodies.
Trying to stop beta-amyloid production.
Anti-tau antibodies.

20
Q

Why are anti-tau treatments less popular?

A

Tau is understood to “go wrong” much later in the progression of AD and therefore it is thought that it might be a bit late to try and address tau dysfunction over amyloid dysfunction.