Dementia
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Basics
Description
Dementia refers to cognitive decline from previous level of performance in various cognitive domains (attention, executive function perceptual-motor, social cognition, language, and memory) interfere significantly with ADLs in the absence of delirium or any other mental disorder.
- DSM-5 classifies dementias under neurocognitive disorders (major and mild) and specifies the cause of neurocognitive decline secondary to the following:
- Alzheimer dementia (AD)
- Vascular dementia (VaD)
- Lewy body dementia
- Parkinson disease dementia
- Frontotemporal dementia
- Creutzfeldt-Jakob disease (CJD)
- HIV dementia
- Substance-/medication-induced neurocognitive disorder
Epidemiology
Incidence
- In 2011, average annual incidence for AD was 0.4% in ages 65 to 74, 3.2% in ages 75 to 84, and 7.6% in ages ≥85.
- Annual incidence of Alzheimer and other dementias expected to double by 2050
Prevalence
- In patients age ≥65 years
- AD: 11.3% (5.3% in ages 65 to 74, 13.8% in ages 75 to 84, 34.6% in ages >85)
- VaD: 1.6%
- Other: 13%
- Estimated 5 to 6 million Americans living with dementia
- Expected to increase to 14 million by 2050
Etiology and Pathophysiology
- AD: involves β-amyloid protein accumulation and/or neurofibrillary tangles (NFTs), synaptic dysfunction, neurodegeneration, and eventual neuronal loss
- Age, genetics, systemic disease, smoking, and other host factors may influence the β-amyloid accumulation and/or the pace of progression toward the clinical manifestations of AD.
- VaD: cerebral atherosclerosis/emboli with clinical/subclinical infarcts
Genetics
- AD: positive family history in 50%, but 90% AD is sporadic: APOE4 increases risk but full role unclear.
- Familial/autosomal dominant AD accounts for <5% AD: amyloid precursor protein (APP), presenilin-1 (PSEN-1), and presenilin-2 (PSEN-2).
Risk Factors
- Age is the strongest factor.
- Sex: female > male
- Genetic predisposition
- Hypertension: AD; VaD
- Hypercholesterolemia: AD; VaD
- Diabetes: VaD
- Obesity: VaD
- Cigarette smoking: VaD
- Endocrine/metabolic abnormalities: hypothyroidism, Cushing syndrome; thiamine and vitamin B12 deficiency
- Chronic alcoholism, other drugs
- Lower educational status
- Head injury early in life
- Sedentary lifestyle
General Prevention
- Treat reversible causes of dementia, such as drug-induced, alcohol-induced, and vitamin deficiencies.
- Treat hypertension, hypercholesterolemia, and diabetes.
- BP control and low-dose aspirin may prevent or lessen cognitive decline in VaD.
- Maintain or increase physical activity and exercise.
- Continue cognitively stimulating activities and social interactions.
Commonly Associated Conditions
- Anxiety and major depression
- Psychosis (delusions; delusions of persecution are common)
- Delirium
- Behavioral disturbances (agitation, aggression)
- Sleep disturbances
-- To view the remaining sections of this topic, please log in or purchase a subscription --
Basics
Description
Dementia refers to cognitive decline from previous level of performance in various cognitive domains (attention, executive function perceptual-motor, social cognition, language, and memory) interfere significantly with ADLs in the absence of delirium or any other mental disorder.
- DSM-5 classifies dementias under neurocognitive disorders (major and mild) and specifies the cause of neurocognitive decline secondary to the following:
- Alzheimer dementia (AD)
- Vascular dementia (VaD)
- Lewy body dementia
- Parkinson disease dementia
- Frontotemporal dementia
- Creutzfeldt-Jakob disease (CJD)
- HIV dementia
- Substance-/medication-induced neurocognitive disorder
Epidemiology
Incidence
- In 2011, average annual incidence for AD was 0.4% in ages 65 to 74, 3.2% in ages 75 to 84, and 7.6% in ages ≥85.
- Annual incidence of Alzheimer and other dementias expected to double by 2050
Prevalence
- In patients age ≥65 years
- AD: 11.3% (5.3% in ages 65 to 74, 13.8% in ages 75 to 84, 34.6% in ages >85)
- VaD: 1.6%
- Other: 13%
- Estimated 5 to 6 million Americans living with dementia
- Expected to increase to 14 million by 2050
Etiology and Pathophysiology
- AD: involves β-amyloid protein accumulation and/or neurofibrillary tangles (NFTs), synaptic dysfunction, neurodegeneration, and eventual neuronal loss
- Age, genetics, systemic disease, smoking, and other host factors may influence the β-amyloid accumulation and/or the pace of progression toward the clinical manifestations of AD.
- VaD: cerebral atherosclerosis/emboli with clinical/subclinical infarcts
Genetics
- AD: positive family history in 50%, but 90% AD is sporadic: APOE4 increases risk but full role unclear.
- Familial/autosomal dominant AD accounts for <5% AD: amyloid precursor protein (APP), presenilin-1 (PSEN-1), and presenilin-2 (PSEN-2).
Risk Factors
- Age is the strongest factor.
- Sex: female > male
- Genetic predisposition
- Hypertension: AD; VaD
- Hypercholesterolemia: AD; VaD
- Diabetes: VaD
- Obesity: VaD
- Cigarette smoking: VaD
- Endocrine/metabolic abnormalities: hypothyroidism, Cushing syndrome; thiamine and vitamin B12 deficiency
- Chronic alcoholism, other drugs
- Lower educational status
- Head injury early in life
- Sedentary lifestyle
General Prevention
- Treat reversible causes of dementia, such as drug-induced, alcohol-induced, and vitamin deficiencies.
- Treat hypertension, hypercholesterolemia, and diabetes.
- BP control and low-dose aspirin may prevent or lessen cognitive decline in VaD.
- Maintain or increase physical activity and exercise.
- Continue cognitively stimulating activities and social interactions.
Commonly Associated Conditions
- Anxiety and major depression
- Psychosis (delusions; delusions of persecution are common)
- Delirium
- Behavioral disturbances (agitation, aggression)
- Sleep disturbances
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