Medicine Central™ is a quick-consult mobile and web resource that includes diagnosis, treatment, medications, and follow-up information on over 700 diseases and disorders, providing fast answers—anytime, anywhere. Explore these free sample topics:
-- The first section of this topic is shown below --
- DSM-5 classifies dementias under neurocognitive disorders (major and mild).
- Evidence of cognitive decline from previous level of performance in one of cognitive domains (attention, executive function perceptual-motor, social cognition and memory). The cognitive deficits interfere significantly with ADLs (for major only) and do not occur exclusively in the context of delirium or any other mental disorder.
- DSM-5 specifies the cause of neurocognitive decline secondary to the following:
- Alzheimer dementia (AD)
- Progressive cognitive decline; most common age >65 years
- Vascular dementia (VaD)
- Usually correlated with a cerebrovascular event and/or cerebrovascular disease
- Stepwise deterioration with periods of clinical plateaus
- Lewy body dementia
- Fluctuating cognition associated with parkinsonism, hallucinations and delusions, gait difficulties, and falls
- Frontotemporal dementia
- Language difficulties, personality changes, and behavioral disturbances
- Creutzfeldt-Jakob disease (CJD)
- Very rare; rapid onset
- HIV dementia
- Substance-/medication-induced neurocognitive disorder
- Alzheimer dementia (AD)
- In patients age ≥65 years
- AD: 5–10% (age 65 to 70 years); 25% (≥70 years)
- VaD: 0.2% (age 65 to 70 years); up to 16% (≥70 years)
- Other: 13%
- Estimated 5.4 million Americans had AD in 2010.
- 5 million >65 years of age; 200,000 <65 years
- Prevalence expected to double by 2030
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
- 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).
- Age; sex: female > male
- Genetic predisposition
- Hypertension: AD; VaD
- Hypercholesterolemia: AD; VaD
- Diabetes: 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
- Treat reversible causes of dementia, such as drug-induced, alcohol-induced, and vitamin deficiencies.
- Treat hypertension, hypercholesterolemia, and diabetes.
- No evidence for statins (or any other specific medication) to prevent onset of dementia (1)[A]
- BP control and low-dose aspirin may prevent or lessen cognitive decline in VaD.
Commonly Associated Conditions
- Anxiety and major depression
- Psychosis (delusions; delusions of persecution are common)
- Behavioral disturbances (agitation, aggression)
- Sleep disturbances