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DEMENTIA 1. Major causes, types, and symptoms of dementia and the clinical course of dementias Symptoms - dementia is a decline in cognitive function measured in relationship to previous levels - general, progressive deficit in memory areas, learning of new information, ability to communicate, and motor coordination - loss of intellect, memory, or mental capacity accompanied by personality and behavior changes - definition of dementia requires presence of multiple deficits including memory impairment and one of the following: aphasia, apraxia, agnosia, or executive functioning deficits (higher cortical); other criterion includes impaired occupational/social functioning Causes/Types - most common causes of dementia include Alzheimer’s disease (50%) and vascular dementia (25%); other causes (25%): degenerative diseases such as Parkinson’s disease, multiple sclerosis, substance abuse, alcohol-induced dementia (Korsakoff Syndrome), infectious diseases, AIDS, encephalitis, autoimmune problems (Lupus), and Down’s Syndrome - Cortical dementia due to damage to neocortex (Alzheimer’s); slowing on tasks and memory encoding - Subcortical dementia due to damage to subcortical structures, such as basal ganglia (Parkinson’s disease); cognitive slowing and memory retrieval problems - Vascular disorders (strokes) cause damage to both cortical and subcortical structures Clinical course - some dementias are reversible (brain tumor), while others are not reversible (Alzheimer’s) - early stages cognitive deficits in 2-3 of areas mentioned above; problems are noticeable, but overall function is good - middle stages more severe cognitive deficits seen in several areas; problems noticeable - late stages almost all cognitive functions impaired with loss of effective motor control; patient requires total care at this point 2. Neuropathological changes that characterize Alzheimer’s disease Neurofibrillary tangles - abnormal meshwork of filamentous material - tangles consist of an abnormally phosphorylated microtubule associated protein called tau - tangles occur within cytoplasm of neuron and impair axonal transport - tangle containing neurons lack functional MTs neural dysfunction and death Senile plaques - extracellular deposits of amyloid proteins surrounded by activated microglia, cytokines, complement proteins, neurites, apolipoprotein E, swollen synaptic terminals and cellular debris - Beta amyloid protein secreted by many cells; it is created from amyloid precursor protein (APP), through protease action - tangles and senile plaques develop with temporal lobe structures initially hippocampus, entorhinal cortex and parahippocampal gyrus; parietal lobe also effected - later frontal cortex and association cortices show pathology; not much damage to subcortical structures - number of synapses in cortex decreases and increased neurofibrillary tangles decline in intellectual function 3. Brain regions that demonstrate prominent changes in dementia - diagnostic changes decrease in blood flow and decrease in glucose utilization in cingulate gyrus, parietal lobes and posterior temporal lobes bilaterally 4. Roles of genes for Alzheimer’s disease - genes located on chromosomes 1, 14, and 21 contribute to development of early-onset Alzheimer’s disease - Almost all Down’s syndrome (trisomy 21) individuals who survive until age 50 develop plaques and tangles - gene for APP (amyloid precursor protein - plaques) on chromosome 21 (may be mutated) - Down’s syndrome more beta amyloid produced earlier onset of plaque formation earlier formation of neuropathological changes - chromosome 19 gene for apolipoprotein E (ApoE): protein involved in lipid transport accounts for 45% of Alzheimer’s cases - 3 alleles E2, E3, E4; E4 allele increases risk for Alzheimer’s; E2 allele has neuroprotective effect - ApoE genotype predicts when, not whether, one is predisposed to develop Alzheimer’s - E4 allele develop symptoms earlier; ApoE effects clearance of beta amyloid produced by neurons; if E4 is present less beta amyloid cleared from brain beta amyloid aggregates into plaques - more amyloid load in brain age of onset of symptoms becomes earlier 5. PET and SPECT findings in Alzheimer’s patients - diagnostic changes decrease in blood flow and decrease in glucose utilization in cingulate gyrus, parietal lobes and posterior temporal lobes bilaterally - can be identified in PET and SPECT scans; can also be used to differentiate Alzheimer’s from other forms of dementia - decrease in glucose utilization precedes cognitive decline and neuropathological changes by 30-40 years - later in illness frontal lobes demonstrate decreased blood flow - primary motor and sensory cortices, and subcortical structures spared