Cognitive Disorders of Aging Flashcards
what functions decrease as a result of neurocognitive disorders of aging?
- sensory - sight, hearing, smelling, tasting, proprioception
- motor - walking, talking, dancing, exercise
- memory - short term, long term, memory recall
- cognitive - speech, learning, reading, writing
- behavior and emotions
describe healthy brain function
- 10 B neurons, each neuron joins a network of other neurons to coordinate different functions
- these functions require an immense amount of energy and oxygen (when something goes wrong in one of these networks, immediate or progressive loss of function occurs due to neuronal death)
describe aging and memory
- minor short term memory los, losing or misplacing items, occasional forgetfulness, forgetting details
- dementias - loss of memory and other mental abilities severe enough to interfere with daily life (cause physical changes in the brain)
what are 7 types of dementias?
- alzheimer’s disease
- vascular dementia
- mixed dementia
- lewy body dementia
- hungington’s disease
- creutzfeldt-jakob disease
- frontotemporal dementia
describe alzheimer’s disease
- alois alzheimer was first to describe “pre-senile” dementia
- characterized by problems in memory, thinking, and behavior great enough to interfere with daily life
- considered a progressive, degenerative disease that worsens over time
describe how alzheimer’s disease worsens over time
- early stage = mild memory loss
- late stage = loss of ability to converse and respond to their environment
what is the average lifespan after initial symptom presentation of a patient with alzheimer’s disease?
about 8 years, but can range from 4-20 years depending on age and general health
what are the neurological findings of alzheimer’s disease?
loss of neurons leads to atrophy of the cortical structure of the brain in the affected regions
what are the histological findings of alzheimer’s disease?
- presence of dense amyloid plaques primarily composed of insoluble beta-amyloid peptides and cellular material around neurons
- presence of neurofibrillary tangles composed of aggregations of microtubule associated tau proteins that accumulate inside the neurons itself
- lewy bodies
what are the biochemical findings of alzheimer’s disease related to amyloid precursor protein?
- amyloid precursor protein (APP) is a transmembrane protein involved in neuron growth, survival, and post injury repair
- APP is cleaved, beta- and gamma-secretase into smaller pieces
- beta amyloid fragments of this protein begin to clump together forming plaques
- inhibition of enzyme function and glucose utilization by neurons is also observed
- apoptosis is triggered = neuronal loss = cortical atrophy
what are the biochemical findings of alzheimer’s disease related to neurofibrillary tangles?
- microtubules (components of the neuronal cytoskeleton) are stabilized by phosphorylated tau proteins
- tau proteins are hyper-phosphorylated, thereby creating clumps or “tangles”
- this causes microtubules to fall apart, thereby losing the cell’s nutrient transport system, and the cell dies
T or F:
most people develop plaques and tangles as they age, but alzheimer’s disease patients develop a much larger amount
true
___ is the most common cause of dementia and represents ___% of all dementia cases
- alzheimer’s
- 60-80%
what is the greatest known risk factor for alzheimer’s disease?
age (but can happen in younger people as well)
alzheimer’s disease is the ___ largest cause of death in the US
6th
___ is caused by inadequate blood flow to the brain which results in localized hypoxia and eventual neuronal death
vascular dementia
hypoxia that results from vascular dementia causes varying degrees of cognitive impairment, which can range from mild to severe. what are some of these impairments?
- memory loss, problems thinking, problems solving, reasoning, speech, word recall, etc.
- confusion, disorientation, attention problems, vision problems, etc.
what are the typical symptoms of vascular dementia?
they vary widely depending on affected brain area
what are the risk factors for vascular dementia?
- advancing age, smoking, cariovascular disease (HTN, hypercholesteremia, etc.), diabetes, lack of exercise, obesity, and alcohol consumption
- same for heart disease
what is the treatment and prevention for vascular dementia?
- addressing risk factors
- some alzheimer’s drugs may help
what is the cause of lewy body dementia?
- unknown
- does not appear to have any association with familial or genetic inheritance
how is lewy body dementia diagnosed?
through autopsy (post mortem)
what is the “hallmark” of lewy body dementia?
- lewy bodies present in histological samples
- alpha-synuclein protein is present but its function is unknown
- present in other dementias including parkinson’s disease and alzheimer’s
- destroys brain cells and gets worse over time
- limits lifespan
what are the symptoms of lewy body dementia?
- changes in cognitive ability (thinking and reasoning)
- confusion and varying alertness
- memory problems
- changes in posture and balance
- autonomic system disturbences
- visual hallucinations
- delusions
- trouble interpreting visual information
- acting out dreams, sometimes violently (REM sleep disorder)
what is the treatment for lewy body dementia?
- address symptoms
- antipsychotic drugs - can cause serious side effects in 50% of patients
- antidepressants - SSRIs
- clonazepam - REM sleep disorder
mixed dementia typically includes characteristics of what other three dementias?
- alzheimers disease, vascular dementia, and lewy body dementia
- plaques, lewy bodies, and vascular changes (blood clots)
T or F:
symptoms of mixed dementia are indistinguishable from other types of dementia
true
when is mixed dementia usually diagnosed?
post mortem
what are the drugs used to treat mixed dementia?
no specific drugs for treating mixed dementia are FDA approved
huntington’s disease is a brain disorder that causes changes in the central brain that affect movement, thinking, and mood, and is caused by a single defective gene in ___
chromosome 4
describe the defective gene in chromosome 4 that causes huntington’s disease
- the gene codes for a protein huntingtin, which when damaged, causes brain changes that lead to the phenotype observed
- normally, this protein contains 17-20 repetitions of a chemical code, but in huntington’s, this protein contains more than 40 repetitions
- the more repeats, the sooner the onset of symptoms and the faster the progression of the disease
when do symptoms of huntington’s disease develop?
between age 30-50 but can appear as early as 2 and late as 80
how can huntington’s disease be diagnosed?
- a genetic test is available to diagnose this disease
- diagnostic tests essentially measure the # of repetitions
is there a cure for huntington’s disease?
no
what is the treatment for huntington’s disease?
- antipsychotics for involuntary muscle movements and SSRIs for anxiety and depression
- several possible treatments are being investigated
- gene silencing (stops production of mutant protein)
- neuronal replacement (stem cells help repair damaged neurons)
___ is a type of dementia caused by a prion protein found int he body that folds into an abnormal shape and causes similar prion proteins to do the same in the brain
creutzfeldt-jakob disease
___ are known as “infectious proteins” that can cause normally folded proteins to misfold
prions
describe creutzfeldt-jakob disease
- similar to bovine spongiform encephalopathy in cows
- fast moving disease that causes dementia that gets worse very quickly
- rare but extremely fatal, as 90% of patients die within one year of diagnosis
- can be passed on by exposure to infected brain or spinal tissue
what are the sources of infection of creutzfeldt-jakob disease?
- medical procedures involving instruments used in neurosurgery, growth hormone from human sources, or certain transplanted human tissues
- consumption of BSE infected beef can cause a variant of CJD
what is the best diagnostic instrument for creutzfeldt-jakob disease?
rapid symtpom progression
is there a cure for creutzfeldt-jakob disease?
no
what is the cause of frontotemporal dementia?
inherited with no apparent risk factors
describe frontotemporal dementia
- neuronal damage leads to functional losses associated with the frontal and temporal regions of the brain
- progressive deterioration of behavior and personality, language, muscle, and motor function
- there are approximately 6 subtypes/variations of this disease
describe the behavior variant of frontotemporal dementia
- severe changes in personality
- nerve cell loss in areas that control conduct, judgement, empathy, and foresight
describe primary progressive aphasia associated with frontotemporal dementia
- semantic variant - patient loses ability to understand or formulate words in a spoken sentence
- non-fluent or agrammatic variant - patient speech is hesitant, labored, or devoid of grammar
what 3 characteristics of frontotemporal dementia affect muscles?
- amyotrophic lateral sclerosis (ALS) - muscle weakness and wasting, effects the motor neurons
- corticobasal syndrome - loss of coordination and stiffening of arms and legs
- progressive supranuclear palsy - muscle stiffness, difficulty walking, changes in posture
what two main types of medications are used to treat neurocognitive disorders?
- cholinesterase inhibitors treat the symptoms but not the source of the disease
- glutamine regulators
describe how cholinesterase inhibitors are used to treat symptoms of neurocognitive disorders
- acetylcholine is a NT involved in learning and memory
- cholinesterase inhibitors prevent acetylcholine from being broken down
- this allows transmission of this chemical between the associated neuronal network to continue
- reduce memory related symptoms
describe how glutamate regulators are used to treat neurocognitive disorders
- glutamate is involved in information processing
- improves mental function and ability to perform activities
what specific medications are used to treat mild to moderate alzheimers? what is the method of action?
- exelon, aricept, razadyne
- inhibits acetylcholine breakdown
what specific medications are used to treat moderate to severe alzheimer’s? what functions do they improve?
- namenda, namenda/namzaric
- improves memory, attention, reason, language, and task performance
in the dental management of patients with neurocognitive disorders, patient assessment should be directed toward ___
understanding the nature, severity, control, and stability of the disease
what are some disease-related oral complications of patients with neurocognitive disorders?
- poor oral hygiene due to decreased ability to perform simple tasks
- increased xerostomia (polypharmacy) - caries
- periodontal disease
- candidiasis
- increased risk for aspiration pneumonia
treatment planning for patients with neurocognitive disorders should be focused on ___
preventing oral disease
- complex tx should be done before moderate to severe stage of dementia
- maintain dental status and minimize deterioration in severe alzheimers
- removable appliances may need to be excluded from tx plan of severe alzheimer’s patients due to risk of self injury
according to the sparks study, ___ may be a risk factor for alzheimer’s disease
periodontitis
the kamer study found an association between periodontal disease and an increased load of ___
beta amyloid plaques
the kamer study hypothesized that periodontally produced ___ may travel into the brain through neural pathways that connect the oral cavity directly to the brain, and that some perio-related microorganisms can invade neural tissue
cytokines
in relation to the kamer study, treponema species are closely related to t. pallidum (syphillus) which have been shown to enter the brain and induce what 3 things in patients with syphillus?
- chronic inflammation
- cortical atrophy
- amyloid depositions
