Source: Abnormal Psychology textbook (University of Florida)
Tags: neurocognitive disorder, NCD, dementia, Alzheimer's disease, vascular NCD, Parkinson's, Lewy body, Huntington's, HIV, delirium, neurofibrillary tangles, plaques, beta-amyloid, tau, acetylcholine, ApoE, sundowning
Difficulty: Intermediate to Advanced Prerequisites: Understanding of brain anatomy (cortex, hippocampus, amygdala, cerebellum, ventricles), neurotransmitter systems (acetylcholine, dopamine, glutamate), and the concept of degenerative disease. Familiarity with the DSM-5 classification system.
Neurocognitive disorders (NCDs) arise later in life and involve cognitive problems such as memory deficits, language disturbances, perceptual disturbances, impaired planning and organising, and failure to recognise objects or people. They can result from degenerative diseases (most commonly Alzheimer's), vascular disease, brain injury, infections, or chronic substance abuse. Delirium is a separate condition characterised by disorientation, memory loss, and clouding of attention, typically arising suddenly and signalling a serious underlying medical problem. This material connects the biological basis of cognition with clinical presentation and is heavily tested because of the ageing population and the clinical importance of distinguishing between NCD types and delirium.
Major and mild neurocognitive disorders involve progressive or acquired cognitive decline affecting memory, language, perception, and executive function. Alzheimer's disease is the most common cause. Delirium is a separate, acute condition marked by sudden disorientation and attentional problems, usually signalling an underlying medical emergency. Treatment options are limited for most NCDs but include cholinesterase inhibitors, behavioural therapies, and prevention strategies.
Major neurocognitive disorder (dementia)
Severe decline in cognitive function sufficient to impair daily functioning, including memory, language, perception, planning, and object/person recognition. In simple terms, the person can no longer remember fundamental facts about their life, express themselves, or carry out basic everyday tasks.
Mild neurocognitive disorder
A milder version of major NCD involving modest cognitive decline from previous performance levels, but without significant impairment in daily functioning. Think of it as a notable but not yet disabling decline.
Aphasia
Deterioration of language ability, including difficulty producing names of objects or people, and sometimes inability to understand what others are saying.
Apraxia
Impairment of the ability to execute common actions (such as waving goodbye), not caused by motor function problems, sensory issues, or failure to comprehend what is required.
Agnosia
Failure to recognise objects or people, worsening as the disorder progresses.
Neurofibrillary tangles
Twisted, tangled filaments within nerve cells in the brain, made of a protein called tau. They impede the movement of nutrients between cells, eventually causing cell death. Common in Alzheimer's but rare in people without NCD.
Plaques (beta-amyloid)
Deposits of beta-amyloid protein (a neurotoxin) that accumulate between cells in the cerebral cortex, hippocampus, amygdala, and other structures critical to memory and cognition.
Apolipoprotein E (ApoE) gene
A gene on chromosome 19 linked to Alzheimer's disease. It regulates the ApoE protein, which transports cholesterol and binds to beta-amyloid. The e4 allele increases risk; inheriting e4 from both parents increases risk further. The e4 allele is associated with reduced cortex and hippocampus volume, greater cognitive deficits, and earlier onset.
Vascular neurocognitive disorder
NCD caused by cerebrovascular disease (blocked blood supply to brain areas causing tissue damage). Can follow a single large stroke or an accumulation of smaller strokes. Characterised by significant declines in processing speed, attention, and executive functions.
Delirium
A condition characterised by disorientation, recent memory loss, and clouding of attention, with sudden onset (hours to days) and short duration (rarely longer than a month). Symptoms fluctuate over the course of a day and often worsen at night (sundowning). Usually signals a serious underlying medical condition.
Sundowning
The tendency for delirium symptoms to fluctuate over the day and worsen at night.
Echolalia (in NCD context)
Repeating what is heard, which can occur in advanced stages of neurocognitive disorder.
Palilalia
Repeating one's own sounds or words over and over again.
Cholinesterase inhibitors
Medications (e.g. donepezil/Aricept, rivastigmine/Exelon, galantamine/Reminyl) that prevent the breakdown of acetylcholine. They have a modest positive effect on NCD symptoms. Side effects include nausea, diarrhoea, and anorexia.
NCDs usually arise later in life.
They result from medical conditions causing cognitive impairment, or from substance intoxication/withdrawal.
Cognitive problems include memory deficits, language disturbances, perceptual disturbances, impaired capacity to plan and organise, and failure to recognise or identify objects.
Major NCD (dementia): cognitive decline severe enough to impair daily functioning. Prevalence increases with age. Can be caused by degenerative diseases (e.g. Alzheimer's), vascular disease, brain injury, progressive diseases, and chronic substance abuse.
Mild NCD: modest decline from previous performance, not yet significantly impairing daily functioning.
Memory deficits that differ from normal forgetting: memory does not return, and the person may not respond to reminders or cues.
May repeat questions, frequently misplace items, try to compensate by writing things down but then forget to check notes.
May become angry or fabricate answers to hide memory loss.
Become lost in familiar places and cannot navigate without help.
Eventually forget major life events, their own history, and even their own name.
Aphasia: difficulty producing names, use of vague references to compensate. May be unable to understand others or follow simple requests.
Echolalia (repeating what is heard) and palilalia (repeating own words) may appear.
Apraxia: cannot execute common actions despite no motor or sensory impairment.
Agnosia: cannot recognise objects or people, worsening over time.
Loss of executive functions: inability to plan, initiate, monitor, and stop complex behaviours (e.g. preparing a meal).
Difficulty with abstract thinking, evaluating new situations, and responding appropriately.
Changes in emotional functioning and personality: depression, decline in judgement, loss of impulse control.
Some deny deterioration, leading to unrealistic or dangerous actions.
Paranoia, accusations of theft, belief that others are conspiring against them.
Violent outbursts and combative behaviours, especially in moderate-to-severe stages.
Most common cause of NCD.
Begins with mild memory loss; memory and disorientation become progressively profound.
Psychiatric symptoms include agitation, dysphoria, apathy, violence, hallucinations, and delusions.
Usually onset after age 65. An early-onset type exists and tends to progress more quickly.
Death typically within 8–10 years of diagnosis, due to physical decline or independent age-related diseases.
Brain abnormalities:
Neurofibrillary tangles (twisted filaments of tau protein within nerve cells) impede nutrient movement between cells, causing cell death. Common in Alzheimer's, rare otherwise.
Plaques (deposits of beta-amyloid) accumulate between cells in the cortex, hippocampus, amygdala, and other memory-critical structures.
Extensive cell death in the cortex leads to cortical shrinkage and enlargement of ventricles. Remaining cells lose many of their dendrites.
Genetic causes:
MZ twin concordance: ~44% (male), ~58% (female). DZ twin concordance: ~25% (male), ~45% (female).
ApoE gene on chromosome 19: the e4 allele increases risk of Alzheimer's, especially when inherited from both parents. Associated with reduced cortex and hippocampus volume, greater cognitive deficits, and earlier onset.
Chromosome 21 is implicated in less common, early-onset forms. People with Down syndrome (trisomy 21) are more likely to develop Alzheimer's, possibly because chromosome 21 is near the amyloid precursor protein gene, and the extra copy may lead to abnormal amyloid production.
Neurotransmitter deficits: acetylcholine (critical for memory), norepinephrine, serotonin, somatostatin, and peptide Y.
Caused by cerebrovascular disease: blood supply to brain areas is blocked, causing tissue damage (detectable by neuroimaging).
Can follow a single large stroke or accumulated small strokes.
Characterised by significant declines in processing speed, attention, and executive functions.
Risk factors: high blood pressure, fatty arterial deposits, diseases that inflame the brain, traumatic brain injury, older age, less education, history of stroke, diabetes.
Medical conditions causing widespread oxygen deficiency (pneumonia, seizures, cardiac arrhythmias) also increase risk.
Parkinson's disease: tremors, muscle rigidity, inability to initiate movement. Results from death of dopamine-producing brain cells. About 75% of people with Parkinson's develop NCD.
Lewy body disease: most common progressive NCD after Alzheimer's. Caused by abnormal round structures in the brain. Features changes in attention, alertness, visual hallucinations, and Parkinson's-like motor symptoms. Related to both Parkinson's and Alzheimer's.
HIV: can cause mild or major NCD. Symptoms include impaired memory and concentration, slowed mental processes, difficulty following conversations, social withdrawal. Progresses to weakness, clumsiness, impaired speech, and eventual confinement to bed. Antiretroviral therapies have reduced new onsets and severity, but more people surviving with HIV means more HIV-related NCDs.
Huntington's disease: rare genetic disorder (ages 25–55). Eventually causes major NCD and chorea (irregular jerks, grimaces, twitches). Transmitted by a single dominant gene on chromosome 4. 50% chance of inheriting if one parent carries the gene.
Prion disease (Creutzfeld-Jakob disease): can cause mild or major NCD, along with brain tremors and other neurological symptoms.
Chronic substance abuse: alcohol, inhalants, and sedatives (especially combined with nutritional deficiencies) can cause NCDs and brain damage. Slow, insidious onset. Can sometimes be slowed with nutritional supplements but is often persistent.
Traumatic brain injury: can cause NCD with changes in cognitive abilities and emotional/personality functioning. Recovery is possible but uncommon. Closed head injuries are typically milder and more likely to resolve. Young men are most susceptible. Soldiers with TBI show NCD-like cognitive decline, depression, aggressive behaviour, long-term unemployment, and social difficulties.
More elderly women than men have Alzheimer's, possibly because women live longer. Women with Alzheimer's tend to show greater cognitive impairment than men.
Black individuals are diagnosed with NCD more often than white individuals, likely due to higher rates of hypertension and cardiovascular disease. Genetic factors for Alzheimer's are more prevalent in white populations.
Lower education levels increase NCD risk, possibly because higher education correlates with higher socioeconomic status, better nutrition, and greater cognitive activity, all of which may build brain resources that delay NCD development.
White families are more likely to hospitalise or institutionalise a family member with NCD. Asian and Latino cultures tend to favour home care, possibly due to financial constraints or stronger cultural norms around family caregiving.
Cholinesterase inhibitors (donepezil, rivastigmine, galantamine): prevent breakdown of acetylcholine. Modest positive effect on symptoms. Side effects: nausea, diarrhoea, anorexia.
Memantine (Namenda): regulates glutamate activity (involved in learning and memory).
Other medications: antidepressants and anti-anxiety drugs for emotional symptoms; antipsychotics for hallucinations, delusions, and agitation. These address secondary symptoms, not primary cognitive decline.
Behaviour therapies: help control anger and emotional instability. Family members can be trained in behavioural techniques for home management, reducing stress, emotional distress, and behaviour problems.
Prevention: aerobic exercise and mental activity may reduce NCD risk. Reducing stroke risk factors lowers the chance of vascular NCD. The "Nun Study" found that greater intellectual activity across the lifespan was associated with milder cognitive impairment even when Alzheimer's pathology was present in the brain.
Characterised by disorientation, recent memory loss, and clouding of attention.
Difficulty focusing, sustaining, or shifting attention.
Most common psychiatric syndrome found in general hospitals.
Signs arise suddenly (hours to days) and are short in duration (rarely longer than a month).
Symptoms fluctuate over the day and often worsen at night (sundowning).
The person may be agitated or frightened, with disrupted sleep-wake cycles, incoherent speech, delusions, and hallucinations.
Progression:
Early phase: fatigue, decreased concentration, irritability, restlessness, or depression
Mild cognitive impairments or perceptual disturbances, visual hallucinations
Orientation becomes disrupted; recognition of familiar people becomes distorted
Immediate memory affected first, then intermediate, then remote memory
Key diagnostic feature: intervals of symptoms alternate with intervals of lucid functioning. Without this alternation, delirium diagnosis is unlikely.
Onset can be dramatic or subtle (an exaggeration of normal character traits, which may go unnoticed).
First indication often comes from observations by family or medical staff.
Delirium usually signals a serious underlying medical condition. If that condition is treated, delirium can be temporary and reversible. The longer delirium continues, the higher the risk of permanent brain damage.
Causes: NCDs, medical disorders, illicit drugs and withdrawal, prescription drug withdrawal, fluid and electrolyte imbalances, medication side effects, toxic substances, post-surgical states (especially in older people), sensory isolation (ICU/CCU psychosis).
Neurotransmitter involvement: acetylcholine, dopamine, serotonin, and GABA levels may be affected.
Risk factors: older age, male sex, pre-existing brain damage or NCD, black individuals (less likely to have health insurance, potentially delaying treatment).
High mortality rates for elderly people with delirium, probably due to the underlying medical conditions.
Treatment:
Recognise and treat immediately
Immediate referral to physician if not already hospitalised
Treat the underlying medical condition first
Discontinue drugs that could be contributing
Antipsychotics to manage confusion and prevent self-harm
In-home nurses or restraints may be needed
A reassuring atmosphere helps reduce agitation
Neurocognitive disorders are among the most pressing public health challenges in ageing populations. Understanding the different types and their causes informs clinical decision-making (e.g. distinguishing Alzheimer's from vascular NCD changes treatment priorities). Recognising delirium quickly is a clinical skill that can prevent permanent brain damage and save lives. The cultural and socioeconomic patterns in NCD caregiving have direct implications for health policy and service design.
Students often think normal age-related forgetfulness is the same as NCD. In NCD, memory does not return even with reminders or cues, and the decline is severe enough to impair daily functioning.
Students sometimes assume Alzheimer's is the only cause of dementia. Vascular disease, Parkinson's, Lewy body disease, Huntington's, HIV, prion disease, substance abuse, and traumatic brain injury can all cause NCDs.
Students may confuse delirium with dementia. Delirium is acute (sudden onset, short duration, fluctuating symptoms with lucid intervals) and often reversible. Dementia is chronic and progressive.
Students sometimes think plaques and tangles are the same thing. Tangles are twisted tau filaments inside nerve cells; plaques are beta-amyloid deposits between cells. Both contribute to Alzheimer's but through different mechanisms.
⚠️ Know the distinction between major and mild NCD: severity of cognitive decline and impact on daily functioning.
⚠️ Be able to list the key symptoms: memory deficits, aphasia, apraxia, agnosia, and loss of executive functions.
⚠️ Alzheimer's pathology: neurofibrillary tangles (tau), plaques (beta-amyloid), cortical shrinkage, ventricular enlargement. Know what each is and how it contributes to symptoms.
⚠️ ApoE gene (chromosome 19), e4 allele, and chromosome 21 link to Down syndrome and Alzheimer's are commonly tested.
⚠️ Distinguish vascular NCD (linked to strokes, cerebrovascular disease) from Alzheimer's (degenerative, plaques and tangles).
⚠️ Delirium versus dementia: know the key differences (onset, duration, fluctuation, reversibility).
⚠️ Sundowning (delirium worsening at night) is a commonly tested detail.
⚠️ Cholinesterase inhibitors (donepezil, rivastigmine, galantamine) and memantine are the main medication classes to know.
True or False: Delirium typically has a gradual onset over months.
Fill in the blank: The protein that makes up neurofibrillary tangles is called ___.
True or False: Vascular NCD is caused by the accumulation of plaques and tangles.
Fill in the blank: The most common cause of major neurocognitive disorder is ___ disease.
True or False: The e4 allele of the ApoE gene is associated with a decreased risk of Alzheimer's.
Answers: 1. False (sudden onset, hours to days). 2. Tau. 3. False (caused by cerebrovascular disease/strokes). 4. Alzheimer's. 5. False (increased risk).
Q: What are the key differences between delirium and major neurocognitive disorder (dementia)?
A: Delirium has a sudden onset (hours to days), short duration (rarely more than a month), fluctuating symptoms with lucid intervals, and is often reversible if the underlying cause is treated. Major NCD has a gradual onset, is chronic and progressive, does not typically have lucid intervals, and is generally irreversible.
Q: Describe the brain abnormalities found in Alzheimer's disease.
A: Neurofibrillary tangles (twisted filaments of tau protein inside nerve cells that impede nutrient transport and cause cell death), plaques (deposits of beta-amyloid between cells in the cortex, hippocampus, amygdala, and other memory-critical structures), and extensive cell death leading to cortical shrinkage, ventricular enlargement, and loss of dendrites.
Q: How does the ApoE gene relate to Alzheimer's disease risk?
A: The ApoE gene on chromosome 19 has three alleles (e2, e3, e4). The e4 allele is associated with higher risk of Alzheimer's, especially when inherited from both parents. It is linked to reduced cortex and hippocampus volume, greater cognitive deficits, and earlier onset. The ApoE protein transports cholesterol and binds to beta-amyloid, potentially playing a role in plaque regulation.
Q: Name three medical conditions other than Alzheimer's that can cause neurocognitive disorders.
A: Parkinson's disease (75% develop NCD), Lewy body disease (most common progressive NCD after Alzheimer's), and Huntington's disease (rare genetic disorder, single dominant gene on chromosome 4). Others include HIV, prion disease, chronic substance abuse, and traumatic brain injury.
Q: What is sundowning, and in which condition is it observed?
A: Sundowning is the tendency for symptoms to fluctuate over the course of a day and worsen at night. It is observed in delirium.
Q: What are cholinesterase inhibitors, and how do they work in treating NCD?
A: Cholinesterase inhibitors (donepezil/Aricept, rivastigmine/Exelon, galantamine/Reminyl) prevent the breakdown of the neurotransmitter acetylcholine, which is critical for memory function. They have a modest positive effect on NCD symptoms. Side effects include nausea, diarrhoea, and anorexia.
NCDs connect to mood disorders because depression frequently co-occurs with cognitive decline, and some NCD symptoms (withdrawal, apathy) mimic depression. Vascular NCD links to health psychology topics about cardiovascular risk factors and stroke prevention. Alzheimer's pathology on chromosome 21 connects back to Down syndrome discussed in the intellectual disability section. Delirium connects to substance use disorders (intoxication and withdrawal as causes) and to hospital-based clinical psychology. The cultural and socioeconomic patterns in NCD prevalence and caregiving tie into broader discussions of health disparities across the course.
Neurocognitive disorder, NCD, dementia, major NCD, mild NCD, Alzheimer's disease, neurofibrillary tangles, tau, plaques, beta-amyloid, ApoE, apolipoprotein E, e4 allele, chromosome 19, chromosome 21, vascular NCD, stroke, cerebrovascular disease, Parkinson's disease, Lewy body disease, Huntington's disease, HIV, prion disease, Creutzfeld-Jakob, traumatic brain injury, TBI, delirium, sundowning, aphasia, apraxia, agnosia, executive function, acetylcholine, cholinesterase inhibitors, donepezil, Aricept, rivastigmine, Exelon, galantamine, Reminyl, memantine, Namenda, glutamate, behaviour therapy, ICU psychosis