What histopathological feature is shown in the CA3 area of the hippocampus in Alzheimer's disease?
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Amyloid plaque.
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What histopathological feature is shown in the CA3 area of the hippocampus in Alzheimer's disease?
Amyloid plaque.
What are neurofibrillary tangles associated with in Alzheimer's disease?
They are a key histopathological feature.
What does granulovacuolar degeneration indicate in Alzheimer's disease?
It is another histopathological change observed.
In which area of the brain are amyloid plaques and neurofibrillary tangles observed in Alzheimer's disease?
CA3 area of the hippocampus.
What is the second most common type of dementia?
Vascular dementia.
What percentage of all dementias does vascular dementia account for?
25%.
What primarily causes cumulative ischaemic brain damage in vascular dementia?
Hypertension and atherosclerosis.
What is the rank of Diffuse Lewy-Body Dementia in terms of commonality?
It is the 3rd most common type of dementia, behind Alzheimer's and Vascular dementia.
What are the two possible onset patterns for vascular dementia?
Sudden onset following a CVA or gradual deterioration after successive CVAs.
What is the aetiology of Diffuse Lewy-Body Dementia?
The aetiology is unknown, but there is a genetic link.
What is dementia?
Acquired global impairment of intellect, but with no altered level of consciousness (ALOC).
What is the rank of Fronto-Temporal Dementias in terms of commonality after Alzheimer's, Vascular, and Lewy-Body dementia?
4th most common dementia.
What is a common morphological finding in vascular dementia on MRI/CT?
Necrotic or fibrotic foci.
What abnormal protein is associated with the pathogenesis of Diffuse Lewy-Body Dementia?
Alpha-synuclein (Lewy Bodies).
What percentage of individuals over 55 years have dementia?
5%.
What is the aetiology of Pick's Disease?
Unknown.
What are some clinical features of vascular dementia?
Memory loss, decreased cognitive function, confusion, mood changes, language problems, executive dysfunction, and rapid shuffling gait.
What is a significant morphological feature of Diffuse Lewy-Body Dementia?
Significant cortical atrophy.
What percentage of individuals over 80 years have dementia?
20%.
What is the primary pathological feature of Fronto-Temporal Dementias?
Selective build-up of Tau proteins within frontal and temporal lobe neurons.
What is the treatment approach for vascular dementia?
There is no cure, but it is preventable.
Where does the cortical atrophy typically start in Diffuse Lewy-Body Dementia?
Around Broca's area.
How does the prevalence of dementia change with age?
It doubles every 5 years beyond age 60.
What are some prevention strategies for vascular dementia?
Control hypertension, reduce cholesterol, control diabetes, stop smoking, and use antiplatelet drugs.
What are the clinical features of Fronto-Temporal Dementias?
Younger patients (40-65 years), dysexecutive syndrome, behavior changes, and language changes.
What percentage of dementia patients have clinically significant behavioral or psychological symptoms?
50%.
What is a defining feature of Pick's Disease compared to Alzheimer's?
Behavior and personality changes occur prior to memory loss in Pick's Disease.
What is the most prevalent early cognitive symptom of dementia?
Memory loss.
What are early clinical features of Diffuse Lewy-Body Dementia?
Fluctuating cognition, vivid visual hallucinations, and impairment in attention.
What type of atrophy is observed in Fronto-Temporal Dementias?
Selective atrophy of frontal and temporal lobes, sparing the parietal and occipital lobes.
What is the most common cause of dementia?
Alzheimer's Disease.
What is the aetiology of Dementia Pugilistica?
Repetitive trauma/concussion.
What are some later non-cognitive symptoms of dementia?
Apathy, depression, delusions, anxiety, agitation, aggression, hallucinations.
What are later clinical features of Diffuse Lewy-Body Dementia?
Parkinsonism, delusions, and transient altered levels of consciousness.
What are the components of the aetiology of Alzheimer's Disease?
Genetic and environmental components; exact aetiology is unknown.
What cognitive function is primarily affected by frontal lobe dysfunction in Fronto-Temporal Dementias?
Executive function.
What are the key pathogenesis factors in Dementia Pugilistica?
Repeated concussive/sub-concussive blows to the head leading to cumulative loss of neurons, fibrosis, hydrocephalus, diffuse axonal injury, and cerebellar damage.
What are the types of primary dementias?
Alzheimer's Disease, Lewy-Body Dementia, Fronto-Temporal Dementia (Pick's Disease), Age-Related (Senile) Dementia.
What type of treatment is promising for Diffuse Lewy-Body Dementia?
Pharmacological treatment with cholinesterase inhibitors.
What type of aphasia is associated with temporal lobe dysfunction in Fronto-Temporal Dementias?
Progressive aphasia (expressive and receptive).
What morphological changes are associated with Dementia Pugilistica?
Hydrocephalus and thinning of the corpus callosum.
What is a key aspect of clinical diagnosis for dementia?
Timeline of symptom progression and impact on activities of daily living (ADLs).
How quickly does Diffuse Lewy-Body Dementia typically onset?
Rapid onset within a few months.
When does memory loss typically occur in Fronto-Temporal Dementias?
Memory is preserved until late stages.
What is the primary aetiology of age-related (senile) dementia?
Old age.
In which syndrome is Alzheimer's Disease inevitable?
Down Syndrome.
What is the Mini-Mental State Examination (MMSE) used for?
To assess cognitive function in dementia diagnosis.
What is a key pathological feature of Alzheimer's Disease?
Excess β-Amyloid protein formation.
What are the clinical features of Dementia Pugilistica?
Slow progression, dementia (decreased memory, cognition, personality changes), parkinsonism (tremors, decreased coordination), unsteady gait, and dysphasias.
What is a key pathological change in age-related dementia?
Neuronal atrophy, particularly in the cortex and hippocampus.
What results from β-Amyloid protein deposition around neurons?
Neuritic plaques.
What is the aetiology of Wernicke's-Korsakoff Syndrome?
Alcohol abuse leading to vitamin B1 (thiamine) deficiency.
What happens to brain mass in age-related dementia?
There is a decrease in brain mass and dendritic branches.
What is a morphological change seen in Alzheimer's Disease?
Severe cortical atrophy.
How does vitamin B1 deficiency affect neuronal health in Wernicke's-Korsakoff Syndrome?
It impairs glucose metabolism, leading to neuronal ATP deficiency and neuronal atrophy, particularly in the cortex and mammillary bodies.
What replaces neurons in age-related dementia?
Glial cells.
Where does cortical atrophy typically start in Alzheimer's Disease?
Around Broca’s area and the frontal area.
What morphological changes are observed in Wernicke's-Korsakoff Syndrome?
Cortical atrophy, mammillary body atrophy and hemorrhages, and cerebellar atrophy.
What is a macro morphological feature of age-related dementia?
Cortical atrophy and enlarging of ventricles (compensatory hydrocephalus).
What is the typical age of onset for Alzheimer's Disease?
As young as 50 years old.
What are the clinical features of Wernicke's-Korsakoff Syndrome?
Impaired memory (anterograde and retrograde), confabulation, vision changes, nystagmus, unequal pupils, and ataxia.
What clinical feature affects all spheres of intellect in age-related dementia?
Dementia.
What is the first sign of Alzheimer's Disease?
Memory loss.
What is the treatment for Wernicke's-Korsakoff Syndrome?
Supplemental thiamine and vitamin B12.
What type of memory loss is typically associated with age-related dementia?
Declarative memory loss.
What is the prognosis for Wernicke's-Korsakoff Syndrome?
Complete recovery is unlikely by the time amnesia and psychosis are apparent.
What are some early progressive signs of Alzheimer's Disease?
Increased memory loss, confusion, apathy, anxiety, and difficulty handling money.
What is anterograde amnesia?
Inability to form new memories from the time of injury/damage onwards.
What late signs indicate extreme global cortical atrophy in Alzheimer's Disease?
Seizures, incontinence, groaning, moaning, or grunting.
What is retrograde amnesia?
Inability to recall memories from the time of injury/damage backwards.
What type of medication is used in the treatment of Alzheimer's Disease?
Acetylcholine-esterase inhibitors.
Which part of the brain is commonly damaged in age-related dementia leading to amnesia?
The hippocampus and/or thalamus.
What is the mean survival time after the onset of Alzheimer's Disease?
7 years.
What is a common cause of death in Alzheimer's Disease patients?
Aspiration pneumonia or other infections.
How is frontotemporal dementia categorised?
Primary progressive aphasia - semantic, progressive nonfluent aphasia
Behavioural variant frontotemporal dementia
How does Behavioural-variant frontotemporal dementia present?
Changes in social conduct and behaviour, loss of empathy, apathy, disinhibition, lack of insight
How does semantic dementia present?
Loss of semantic knowledge, impaired word comprehension and object naming, fluent speech with spared repetition
How does progressive nonfluent aphasia present?
Apraxia and effortful speech, spared object knowledge and word comprehension
Which other degenerative disease is fronto-temporal dementia associated with?
Motor neurone disease (ALS)
