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202: Theme 1 > Dementia > Flashcards

Dementia Flashcards

1
Q

Give four main types of Dementia disorders

A
  • Alzheimer’s disease
  • Dementia with Lewy bodies
  • Frontotemporal dementia
  • Vascular dementia
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2
Q

What are the two ways to look at the Neuropathlogically presentations of dementia

A
  • Microscopically
    • Intra neuronal inclusion bodies
    • Extra neuronal changes (plaques)
  • Macroscopically
    • Generalised brain atrophy
    • Region specific atrophy depending on dementia disorder
    • Enlarged ventricles
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3
Q

Give some microscopic causes of Dementia

A
  • Misfolding of proteins
  • Abnormal accumulation
  • Neuroinflammatory environment
    • Damaged neurons
      • Cell death
  • Proteins involved:
    • Amyloid
    • Tau
    • Synuclein
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4
Q

What dementia disease is caused by Tau abnormalities?

A
  • Alzheimer’s disease
    • can also be caused by Amyloid abnormalities
  • Frontotemporal dementia
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5
Q

What is Tau?

A
  • a highly soluble protein found mostly in the brain
  • it is mostly present in axons
  • it has 6 isoforms and disease process lead to hyperphosphorylated forms of the protein

Functions

  • modulate the stability of axonal microtubules
  • transport
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6
Q

Abnormalities in Tau

A

Hyperphosphorylated forms of Tau

  • Paired helical filaments (PHF)
  • Neurofibrillary tangles (NFTs)
  • PHFs –> NFTs –> Neurodegeneration
    ​
  • Phosphorylation of tau is regulated by activated kinases
    • Hyperphosphorylation of tau can result in the self-assembly of tangles of paired helical filaments (PHF).
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7
Q

Explain Neurofibrillary tangles

A

Described by Alois Alzheimer: consist of paired 10-nanometer diameter filaments twisted around each other in a helical manner (paired helical filaments HF)

  • Seen in neurons after staining
    • Hematoxylin
    • Eosin
    • Bielschowsky
    • Bodian
    • Congo red
  • Most commonly found in temporal lobe structures
    • Hippocampus
    • Amygdala
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8
Q

Amyloid Precursor Protein (APP) in normal and diseased brains

A
  • APP is a transmembrane glycoprotein which is broken down and eliminated in normal brain
  • APP is split by enzymes ß-secretase then y-secretase.
  • ß-amyloid is a peptide of 39–43 amino acids
    • Most common isoforms are Aβ40 and Aβ42
  • Aβ40 is more common of the two, but Aβ42 is the more fibrillogenic and is thus associated with disease states.
  • Fragments accumulate to form plaques, the build-up of ß-amyloid plaques cause neuronal damage
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9
Q

Frontotemporal Dementia (FTD)

A
  • Tau pathology, Pick’s disease described by Arnold Pick 1892
  • Pick bodies
    • rounded, microscopic structures found within neurons
    • Aggregates of tau
  • Hirano bodies
  • Neurons swell, taking on a “ballooned” appearance. Hence, called balloon cells.
  • Plaques and tangles are not found in Pick’s disease.
  • FTD is present in frontal and anterior temporal lobes.
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10
Q

What are Synuclein abnormalities?

A
  • Parkinson disease
  • Dementia with Lewy bodies
  • Fibrillary aggregates of alpha-synuclein protein
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11
Q

What are Synuclein?

A
  • Small, presynaptic neuronal proteins comprised of α-, β-, γ-synucleins of which only α-synuclein aggregates
  • Proteins of 140 amino acids, that is expressed predominantly in neurons
  • Found in neurons and glial cells
  • Function as lipid vesicle binding, inhibition of phospholipase D2 and protein kinase C, dopamine uptake and as a chaperone have been ascribed to α-synuclein.
  • Predominantly expressed in neocortex, hippocampus, substantia nigra and cerebellum.
  • Can aggregate to form intracytoplasmic inclusions in neurons (Lewy bodies).
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12
Q

What are Lewy bodies?

A
  • Spherical, intranuclear, cytoplasmic eosinophilic inclusions
  • Abnormally truncated and phosphorylated neurofilament proteins
  • Contain:
    • Alpha-synuclein
    • Ubiquitin
    • Associated enzymes.
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13
Q

Vascular dementia

A
  • Can result from ischemic or hemorrhagic brain damage.
  • The three most common mechanisms causing disease
    • Single, strategically placed infarcts
    • multiple cortical infarcts
    • subcortical small-vessel disease.
  • Clinical deficits are determined by the size, location, and type of cerebral damage.
  • Because of the variety of pathogenic mechanisms involved in vascular dementia, clinical manifestations can vary.
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14
Q

What steps need to be taking to reach a diagnostic conclusion of a Dementia disease?

A
  • History
  • Examination
  • Bloods/ECG
  • Neuropsychological
  • Behavioural/Activities of Daily Living
  • Neuroimaging
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15
Q

What examinations are done when Dementia is a differential diagnosis?

A
  • General examination
  • Neurological examination
  • Mental State Examination
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16
Q

What bloods/ ECG would be taken for a neurological consultation?

A
  • FBC
  • ESR
  • U/Es
  • LFT
  • TFT
  • B12/folate
  • Syphilis serology
  • ECG
17
Q

What Imaging can be done during a neurologic consultation?

A
  • CT
  • MRI
  • SPECT
  • PET
18
Q

What treatment can be given for Alzheimer’s dementia?

A
  • Donepezil,
  • Rivastigmine,
  • Galantamine,
  • Memantine
19
Q

What treatment can be given for Vascular Dementia

A
  • Identify & Treat vascular risk factors
    • Hypertension
    • Diabetes
    • Hyperlipidaemia
    • AF
    • Carotid disease
  • put patients on anticoagulants
20
Q

Treatment for Frontotemporal dementia

A
  • SSRI antidepressants
21
Q

Treatment for Dementia with Lewy Bodies

A
  • Donepezil
  • Rivastigmine
22
Q

What are future management strategies for dementia?

A
  • Prevention
  • Slow down progression
  • Introduce disease-modifying treatment
  • Cure

Overall support patients to live well with dementia

23
Q

What are the fixed risk factors for dementia?

A
  • Age
  • Genetics
  • Brain injury
  • Education level
  • Alcoholism
24
Q

What are changeable risk factors fro dementia?

A
  • Diabetes
  • Hypertension
  • Brain injury
  • Sleep disorders
  • Depression
  • Obesity
  • Physical Health
25
Q

What methods can be used to slow down the progression of dementia?

A
  • Use available drugs: Donepezil, Rivastigmine, Galantamine, Memantine, Huperzine A
  • Psychological support
  • Lifestyle changes: Vitamins B12 and D, diet, exercise, cognitive stimulation
  • Timely diagnosis and treatment of physical and mental health conditions
26
Q

The use of Vitamin E in dementia treatment

27
Q

The use of NSAIDs in Dementia treatment

A
  • many side effects
    *
28
Q

The use of Ginkgo Biloba in Dementia treatment

A
  • Extract EGb 761
  • 17 active metabolites; 3 antioxidants
  • Dose: 120-240 mg
  • Side Effects
    • Allergy
    • Bleeding
    • Skin reactions
    • GIT
    • Drug interaction
29
Q

What other variables cause an acceleration in decline?

A
  • Psychosis
  • Anti-psychotic treatment
  • Depression
  • Delirium
  • Infections
  • Anaesthesia
  • Decreased cognitive reserve
  • Physical Inactivity
  • Genetic status
  • Age
  • Polypharmacy
  • Hypothyroidism/vitamins deficiency?
30
Q

What methods can be used to modify the disease?

A

Targeting the Tau and Amyloid proteins that misfold and accumulate in the brains of patients with AD

  • Anti-amyloid treatment:
    • destroys existing amyloid plaques: Bapineuzumab, Solanezumab, Crenezumab & Gantenerumab
      • ​CNS clearance hypothesis
      • peripheral sink hypothesis
    • stops aggregation: through agents blocking or modulating beta and gamma secretases
  • Anti-Tau treatment
    • reformulated methylene blue
    • reduces levels of aggregated or misfolded Tau proteins

202: Theme 1 (14 decks)

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