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Alzheimer's disease
Progressive, neurodegenerative disease characterized by memory loss

Alzheimer's disease (AD) is a neurodegenerative disease causing 60–70% of dementia cases, usually starting with difficulty in remembering recent events. It progresses to include language problems, disorientation, mood swings, and behavioral issues. The disease involves accumulation of malformed protein deposits such as amyloid plaques and neurofibrillary tangles, leading to neuron degeneration. Diagnosis combines history, cognitive testing, and imaging. While no treatments stop progression, lifestyle factors like healthy diet and physical activity may help. AD affects about 50 million people globally and is the seventh leading cause of death. Large-scale research programs by the US NIH and the European Union aim to advance understanding and treatment.

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Signs and symptoms

The course of Alzheimer's is generally described in three stages, with a progressive pattern of cognitive and functional impairment.3738 The three stages are described as early or mild, middle or moderate, and late or severe.39 The disease is known to target the hippocampus which is associated with memory, and this is responsible for the first symptoms of memory impairment. As the disease progresses so does the degree of memory impairment.40

First symptoms

The first symptoms are often mistakenly attributed to aging or stress.41 Detailed neuropsychological testing can reveal mild cognitive difficulties up to eight years before a person fulfills the clinical criteria for diagnosis of Alzheimer's disease.42 These early symptoms can affect the most complex activities of daily living.43 The most noticeable deficit is short term memory loss, which shows up as difficulty in remembering recently learned facts and inability to acquire new information.44

Subtle problems with the executive functions of attentiveness, planning, flexibility, and abstract thinking, or impairments in semantic memory (memory of meanings, and concept relationships) can also be symptomatic of the early stages of Alzheimer's disease.45 Apathy and depression can be seen at this stage, with apathy remaining as the most persistent symptom throughout the course of the disease.4647 People with objective signs of cognitive impairment, but not more severe symptoms, may be diagnosed with mild cognitive impairment (MCI). If memory loss is the predominant symptom of MCI, it is termed amnestic MCI and is frequently seen as a prodromal or early stage of Alzheimer's disease.48 Amnestic MCI has a greater than 90% likelihood of being associated with Alzheimer's.49

Early stage

In people with Alzheimer's disease, the increasing impairment of learning and memory eventually leads to a definitive diagnosis. In a small percentage, difficulties with language, executive functions, perception (agnosia), or execution of movements (apraxia) are more prominent than memory problems.50 Alzheimer's disease does not affect all memory capacities equally. Older memories of the person's life (episodic memory), facts learned (semantic memory), and implicit memory (the memory of the body on how to do things, such as using a fork to eat or how to drink from a glass) are affected to a lesser degree than new facts or memories.5152

Language problems are mainly characterised by a shrinking vocabulary and decreased word fluency, leading to a general impoverishment of oral and written language.5354 In this stage, the person with Alzheimer's is usually capable of communicating basic ideas adequately.555657 While performing fine motor tasks such as writing, drawing, or dressing, certain movement coordination and planning difficulties (apraxia) may be present; however, they are commonly unnoticed.58 As the disease progresses, people with Alzheimer's disease can often continue to perform many tasks independently; however, they may need assistance or supervision with the most cognitively demanding activities.59

Middle stage

Progressive deterioration eventually hinders independence, with subjects being unable to perform most common activities of daily living.60 Speech difficulties become evident due to an inability to recall vocabulary, which leads to frequent incorrect word substitutions (paraphasias). Reading and writing skills are also progressively lost.6162 Complex motor sequences become less coordinated as time passes and Alzheimer's disease progresses, so the risk of falling increases.63 During this phase, memory problems worsen, and the person may fail to recognise close relatives.64 Long-term memory, which was previously intact, becomes impaired.65

Behavioral and neuropsychiatric changes become more prevalent. Common manifestations are wandering, irritability and emotional lability, leading to crying, outbursts of unpremeditated aggression, or resistance to caregiving.66 Sundowning can also appear.67 Approximately 30% of people with Alzheimer's disease develop illusionary misidentifications and other delusional symptoms.68 Subjects also lose insight of their disease process and limitations (anosognosia).69 Urinary incontinence can develop.70 These symptoms create stress for relatives and caregivers, which can be reduced by moving the person from home care to other long-term care facilities.7172

Late stage

During the final stage, known as the late-stage or severe stage, there is complete dependence on caregivers.737475 Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech.7677 Despite the loss of verbal language abilities, people can often understand and return emotional signals. Although aggressiveness can still be present, extreme apathy and exhaustion are much more common symptoms. People with Alzheimer's disease will ultimately not be able to perform even the simplest tasks independently; muscle mass and mobility deteriorates to the point where they are bedridden and unable to feed themselves. The cause of death is usually an external factor, such as infection of pressure ulcers or pneumonia, not the disease itself.78 In some cases, there is a paradoxical lucidity immediately before death, where there is an unexpected recovery of mental clarity.79

Causes

Alzheimer's disease is believed to occur when abnormal amounts of amyloid beta (Aβ), accumulating extracellularly as amyloid plaques and tau proteins, or intracellularly as neurofibrillary tangles, form in the brain, affecting neuronal functioning and connectivity, resulting in a progressive loss of brain function.8081 This altered protein clearance ability is age-related, regulated by brain cholesterol,82 and associated with other neurodegenerative diseases.8384

The cause for most Alzheimer's cases is still mostly unknown,85 except for 1–2% of cases where deterministic genetic differences have been identified.86 Several competing hypotheses attempt to explain the underlying cause; the most predominant hypothesis is the amyloid beta (Aβ) hypothesis.87

In the 1970s, the cholinergic hypothesis proposed that Alzheimer's disease is caused by reduced synthesis of the neurotransmitter acetylcholine.88 The loss of cholinergic neurons noted in the limbic system and cerebral cortex, is a key feature in the progression of Alzheimer's.89 The 1991 amyloid hypothesis postulated that extracellular amyloid beta (Aβ) deposits are the fundamental cause of the disease.9091 Support for this postulate comes from the location of the gene for the amyloid precursor protein (APP) on chromosome 21, together with the fact that people with trisomy 21 (Down syndrome) who have an extra gene copy almost universally exhibit at least the earliest symptoms of Alzheimer's disease by 40 years of age.92 A specific isoform of apolipoprotein, APOE4, is a major genetic risk factor for Alzheimer's disease.93 While apolipoproteins enhance the breakdown of amyloid beta, some isoforms are not very effective at this task (such as APOE4), leading to excess amyloid buildup in the brain.94

Genetic

Late onset

Late-onset Alzheimer's is about 70% heritable.9596 Genetic models in 2020 predict Alzheimer's disease with 90% accuracy.97 Most cases of Alzheimer's are not familial, and so they are termed sporadic Alzheimer's disease.98 Of the cases of sporadic Alzheimer's disease, most are classified as late onset where they are developed after the age of 65 years.99

The strongest genetic risk factor for sporadic Alzheimer's disease is APOEε4.100 APOEε4 is one of four alleles of apolipoprotein E (APOE). APOE plays a major role in lipid-binding proteins in lipoprotein particles and the ε4 allele disrupts this function.101 Between 40% and 80% of people with Alzheimer's disease possess at least one APOEε4 allele.102 The APOEε4 allele increases the risk of the disease by three times in heterozygotes and by 15 times in homozygotes.103 Like many human diseases, environmental effects and genetic modifiers result in incomplete penetrance. For example, Nigerian Yoruba people do not show the relationship between dose of APOEε4 and incidence or age-of-onset for Alzheimer's disease seen in other human populations.104105

Early onset

Further information: Early-onset Alzheimer's disease

Only 1–2% of Alzheimer's cases are inherited due to autosomal dominant effects, as Alzheimer's is highly polygenic. When the disease is caused by autosomal dominant variants, it is known as early onset familial Alzheimer's disease, which is rarer and has a faster rate of progression.106 Less than 5% of sporadic Alzheimer's disease have an earlier onset,107 and early-onset Alzheimer's is about 90% heritable.108109 Familial Alzheimer's disease usually implies two or more persons affected in one or more generations.110111112

Early onset familial Alzheimer's disease can be attributed to mutations in one of three genes: those encoding amyloid-beta precursor protein (APP) and presenilins PSEN1 and PSEN2.113 Most mutations in the APP and presenilin genes increase the production of a small protein called amyloid beta (Aβ)42, which is the main component of amyloid plaques.114 Some of the mutations merely alter the ratio between Aβ42 and the other major forms—particularly Aβ40—without increasing Aβ42 levels in the brain.115 Two other genes associated with autosomal dominant Alzheimer's disease are ABCA7 and SORL1.116

Alleles in the TREM2 gene have been associated with a three to five times higher risk of developing Alzheimer's disease.117

A Japanese pedigree of familial Alzheimer's disease was found to be associated with a deletion mutation of codon 693 of APP.118 This mutation and its association with Alzheimer's disease was first reported in 2008,119 and is known as the Osaka mutation. Only homozygotes with this mutation have an increased risk of developing Alzheimer's disease. This mutation accelerates Aβ oligomerization but the proteins do not form the amyloid fibrils that aggregate into amyloid plaques, suggesting that it is the Aβ oligomerization rather than the fibrils that may be the cause of this disease. Mice expressing this mutation have all the usual pathologies of Alzheimer's disease.120

Hypotheses

Amyloid beta and tau protein

The tau hypothesis proposes that tau protein abnormalities initiate the disease cascade.121 In this model, hyperphosphorylated tau begins to pair with other threads of tau as paired helical filaments. Eventually, they form neurofibrillary tangles inside neurons.122 When this occurs, the microtubules disintegrate, destroying the structure of the cell's cytoskeleton which collapses the neuron's transport system.123

A number of studies connect the misfolded amyloid beta and tau proteins associated with the pathology of Alzheimer's disease, as bringing about oxidative stress that leads to neuroinflammation.124 This chronic inflammation is also a feature of other neurodegenerative diseases including Parkinson's disease, and ALS.125 Spirochete infections have also been linked to dementia.126 DNA damages accumulate in Alzheimer's diseased brains; reactive oxygen species may be the major source of this DNA damage.127

Sleep

Sleep disturbances are seen as a possible risk factor for inflammation in Alzheimer's disease.128 Sleep disruption was previously only seen as a consequence of Alzheimer's disease, but as of 2020[update], accumulating evidence suggests that this relationship may be bidirectional.129130

Metal toxicity, smoking, neuroinflammation and air pollution

The cellular homeostasis of biometals such as ionic copper, iron, and zinc is disrupted in Alzheimer's disease, though it remains unclear whether this is produced by or causes the changes in proteins.131132 Smoking is a significant Alzheimer's disease risk factor.133 Systemic markers of the innate immune system are risk factors for late-onset Alzheimer's disease.134 Exposure to air pollution may be a contributing factor to the development of Alzheimer's disease.135

Age-related myelin decline

Retrogenesis is a medical hypothesis that just as the fetus goes through a process of neurodevelopment beginning with neurulation and ending with myelination, the brains of people with Alzheimer's disease go through a reverse neurodegeneration process starting with demyelination and death of axons (white matter) and ending with the death of grey matter.136 Likewise the hypothesis is, that as infants go through states of cognitive development, people with Alzheimer's disease go through the reverse process of progressive cognitive impairment.137

According to one theory, dysfunction of oligodendrocytes and their associated myelin during aging contributes to axon damage, which in turn generates in amyloid production and tau hyperphosphorylation.138139 Comorbidities between the demyelinating disease, multiple sclerosis, and Alzheimer's disease have been reported.140

Other hypotheses

See also: Cell cycle hypothesis of Alzheimer's disease and Ion channel hypothesis of Alzheimer's disease

The association with celiac disease is unclear, with a 2019 study finding no increase in dementia overall in those with celiac disease while a 2018 review found an association with several types of dementia including Alzheimer's disease.141142

Studies have shown a potential link between infection with certain viruses and developing Alzheimer's disease later in life.143 Notably, a large scale study conducted on 6,245,282 patients has shown an increased risk of developing Alzheimer's disease following COVID-19 infection in cognitively normal individuals over 65.144

Some evidence suggests that some viral infections such as Herpes simplex virus 1 (HSV-1) may be associated with dementia, but there are conflicting results and the association with Alzheimer's is unclear as of 2024.145146147

Some researchers have proposed that Alzheimer's disease is Type 3 diabetes because of a number of correspondences with both Type 1 and Type 2 diabetes.148

Pathophysiology

Neuropathology

Alzheimer's disease is characterised by loss of neurons and synapses in the cerebral cortex and certain subcortical regions. This loss results in gross atrophy of the affected regions, including degeneration in the temporal lobe and parietal lobe, and parts of the frontal cortex and cingulate gyrus.149 Degeneration is also present in brainstem nuclei particularly the locus coeruleus in the pons.150 Studies using MRI and PET have documented reductions in the size of specific brain regions in people with Alzheimer's disease as they progressed from mild cognitive impairment to Alzheimer's disease, and in comparison with similar images from healthy older adults.151152

Both Aβ plaques and neurofibrillary tangles are clearly visible by microscopy in brains of those with Alzheimer's disease,153 especially in the hippocampus.154 However, Alzheimer's disease may occur without neurofibrillary tangles in the neocortex.155 Plaques are dense, mostly insoluble deposits of amyloid beta peptide and cellular material outside and around neurons. Neurofibrillary tangles are aggregates of the microtubule-associated protein tau which has become hyperphosphorylated and accumulate inside the cells themselves. Although many older individuals develop some plaques and tangles as a consequence of aging, the brains of people with Alzheimer's disease have a greater number of them in specific brain regions such as the temporal lobe.156 Lewy bodies are not rare in the brains of people with Alzheimer's disease.157

Biochemistry

Main article: Biochemistry of Alzheimer's disease

Amyloid beta

Alzheimer's disease has been identified as a protein misfolding disease, a proteopathy, caused by the accumulation of abnormally folded amyloid beta protein into amyloid plaques, and tau protein into neurofibrillary tangles in the brain.158 Plaques are made up of small peptides, 39–43 amino acids in length, called amyloid beta. Amyloid beta is a fragment from the larger amyloid-beta precursor protein (APP) a transmembrane protein that penetrates the cell's membrane. APP is critical to neuron growth, survival, and post-injury repair.159 In Alzheimer's disease, gamma secretase and beta secretase act together in a proteolytic process which causes APP to be divided into smaller fragments.160 Although commonly researched as neuronal proteins, APP and its processing enzymes are abundantly expressed by other brain cells. One of these fragments gives rise to fibrils of amyloid beta, which then form clumps that deposit outside neurons in dense formations known as amyloid plaques.161 Excitatory neurons are known to be the major producers of amyloid beta that contribute to major extracellular plaque deposition.162

Phosphorylated tau

Alzheimer's disease is also considered a tauopathy due to abnormal aggregation of the tau protein. Every neuron has a cytoskeleton, an internal support structure partly made up of structures called microtubules. These microtubules act like tracks, guiding nutrients and molecules from the body of the cell to the ends of the axon and back. A protein called tau stabilises the microtubules when phosphorylated, and is therefore called a microtubule-associated protein. In Alzheimer's disease, tau undergoes chemical changes, becoming hyperphosphorylated; it then begins to pair with other threads, creating neurofibrillary tangles and disintegrating the neuron's transport system.163 Pathogenic tau can also cause neuronal death through transposable element dysregulation.164 Necroptosis has also been reported as a mechanism of cell death in brain cells affected with tau tangles.165166

Disease mechanism

Exactly how disturbances of production and aggregation of the beta-amyloid peptide give rise to the pathology of Alzheimer's disease is not known.167168 The amyloid hypothesis traditionally points to the accumulation of beta-amyloid peptides as the central event triggering neuron degeneration. Accumulation of aggregated amyloid fibrils, which are believed to be the toxic form of the protein responsible for disrupting the cell's calcium ion homeostasis, induces programmed cell death (apoptosis).169 It is also known that Aβ selectively builds up in the mitochondria in the cells of Alzheimer's-affected brains, and it also inhibits certain enzyme functions and the utilisation of glucose by neurons.170

Evidence supports Aβ as playing a central role in the pathogenesis of AD, but it does not completely explain the condition, as individuals may have normal cognition and very high Aβ burden in their brains at an advanced age,[medical citation needed] and the beneficial effect of therapeutics (such as monoclonal antibodies) promoting Aβ clearance has ranged from nonexistent to modest.171

Iron dyshomeostasis is linked to disease progression, an iron-dependent form of regulated cell death called ferroptosis could be involved. Products of lipid peroxidation are also elevated in AD brain compared with controls.172

Various inflammatory processes and cytokines may also have a role in the pathology of Alzheimer's disease. Inflammation is a general marker of tissue damage in any disease, and may be either secondary to tissue damage in Alzheimer's disease or a marker of an immunological response.173 There is increasing evidence of a strong interaction between the neurons and the immunological mechanisms in the brain. Obesity and systemic inflammation may interfere with immunological processes which promote disease progression.174

Alterations in the distribution of different neurotrophic factors and in the expression of their receptors such as the brain-derived neurotrophic factor (BDNF) have been described in Alzheimer's disease.175176

Evidence has accrued for microglia as central actors in the mechanism of AD.177 Microglia are topographically associated with pTau and Aβ within the brain, even when each pathologic component occurs in distinct brain regions,178 and microglial activation has been documented in those with mild cognitive impairment, despite a lack of tracer uptake, suggesting that microglial dysfunction may precede plaque deposition as an inciting event in AD.179 Microglia are the principal immunological cells of the central nervous system, serving as the tissue-resident macrophages of the brain; they are capable of recognizing and taking up Aβ through multiple pattern recognition receptors, making them central to amyloid clearance within the brain.180 However, microglia can also be a major source of pro-inflammatory mediators which can be deleterious to neurological function.181

Diagnosis

See also: Early-onset Alzheimer's disease § Diagnosis

Alzheimer's disease (AD) can only be definitively diagnosed with autopsy findings; in the absence of autopsy, clinical diagnoses of AD are "possible" or "probable", based on other findings.182183184 Up to 23% of those clinically diagnosed with AD may be misdiagnosed and may have pathology suggestive of another condition with symptoms that mimic those of AD.185

AD is usually clinically diagnosed based on a person's medical history, observations from friends or relatives, and behavioral changes. The presence of characteristic neuropsychological changes with impairments in at least two cognitive domains that are severe enough to affect a person's functional abilities are required for the diagnosis. Domains that may be impaired include memory (most commonly impaired), language, executive function, visuospatial functioning, or other areas of cognition. The neurocognitive changes must be a decline from a prior level of function and the diagnosis requires ruling out other common causes of neurocognitive decline.186187188 Advanced medical imaging with computed tomography (CT) or magnetic resonance imaging (MRI), and with single-photon emission computed tomography (SPECT) or positron emission tomography (PET), can be used to help exclude other cerebral pathology or subtypes of dementia.189 On MRI or CT, Alzheimer's disease usually shows a generalised or focal cortical atrophy, which may be asymmetric. Atrophy of the hippocampus is also commonly seen. Brain imaging commonly also shows cerebrovascular disease, most commonly previous strokes (small or large territory strokes), and this is thought to be a contributing cause of many cases of dementia (up to 46% cases of dementia also have cerebrovascular disease on imaging).190 FDG-PET scan is not required for the diagnosis but it is sometimes used when standard testing is unclear. FDG-PET shows a bilateral, asymetric, temporal and parietal reduced activity.191 Advanced imaging may predict conversion from prodromal stages (mild cognitive impairment) to Alzheimer's disease.192 FDA-approved radiopharmaceutical diagnostic agents used in PET for Alzheimer's disease are florbetapir (2012), flutemetamol (2013), florbetaben (2014), and flortaucipir (2020).193 Because many insurance companies in the United States do not cover this procedure, its use in clinical practice is largely limited to clinical trials as of 2018[update].194

Assessment of intellectual functioning including memory testing can further characterise the state of the disease.195 Medical organizations have created diagnostic criteria to ease and standardise the diagnostic process for practising physicians. Definitive diagnosis can only be confirmed with post-mortem evaluations when brain material is available and can be examined histologically for senile plaques and neurofibrillary tangles.196197

Criteria

There are three sets of criteria for the clinical diagnoses of the spectrum of Alzheimer's disease: the 2013 fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5); the National Institute on Aging-Alzheimer's Association (NIA-AA) definition as revised in 2011; and the International Working Group criteria as revised in 2010.198199

Eight intellectual domains are most commonly impaired in AD—memory, language, perceptual skills, attention, motor skills, orientation, problem solving and executive functional abilities, as listed in the fourth text revision of the DSM (DSM-IV-TR).200

The DSM-5 defines criteria for probable or possible AD for both major and mild neurocognitive disorder.201202203 Major or mild neurocognitive disorder must be present along with at least one cognitive deficit for a diagnosis of either probable or possible AD.204205 For major neurocognitive disorder due to AD, probable Alzheimer's disease can be diagnosed if the individual has genetic evidence of AD206 or if two or more acquired cognitive deficits, and a functional disability that is not from another disorder, are present.207 Otherwise, possible AD can be diagnosed as the diagnosis follows an atypical route.208 For mild neurocognitive disorder due to AD, probable Alzheimer's disease can be diagnosed if there is genetic evidence, whereas possible AD can be met if all of the following are present: no genetic evidence, decline in both learning and memory, two or more cognitive deficits, and a functional disability not from another disorder.209210

The NIA-AA criteria are used mainly in research rather than in clinical assessments.211 They define AD through three major stages: preclinical, mild cognitive impairment (MCI), and Alzheimer's dementia.212213 Diagnosis in the preclinical stage is complex and focuses on asymptomatic individuals;214215 the latter two stages describe individuals experiencing symptoms,216 along with biomarkers,217 predominantly those for neuronal injury (mainly tau-related) and amyloid beta deposition.218219 The core clinical criteria itself rests on the presence of cognitive impairment220 without the presence of comorbidities.221222 The third stage is divided into probable and possible AD dementia.223 In probable AD dementia there is steady impairment of cognition over time and a memory-related or non-memory-related cognitive dysfunction.224 In possible AD dementia, another causal disease such as cerebrovascular disease is present.225

Techniques

Neuropsychological tests including cognitive tests such as the mini–mental state examination (MMSE), the Montreal Cognitive Assessment (MoCA) and the Mini-Cog are widely used to aid in diagnosis of the cognitive impairments in AD.226 These tests may not always be accurate, as they lack sensitivity to mild cognitive impairment, and can be biased by language or attention problems;227 more comprehensive test arrays are necessary for high reliability of results, particularly in the earliest stages of the disease.228229

Further neurological examinations are crucial in the differential diagnosis of Alzheimer's disease and other diseases.230 Interviews with family members are used in assessment; caregivers can supply important information on daily living abilities and on the decrease in the person's mental function.231 A caregiver's viewpoint is particularly important, since a person with Alzheimer's disease is commonly unaware of their deficits.232 Many times, families have difficulties in the detection of initial dementia symptoms and may not communicate accurate information to a physician.233

Supplemental testing can rule out other potentially treatable diagnoses and help avoid misdiagnoses.234 Common supplemental tests include blood tests, thyroid function tests, as well as tests to assess vitamin B12 levels, rule out neurosyphilis and rule out metabolic problems (including tests for kidney function, electrolyte levels and for diabetes).235 MRI or CT scans might also be used to rule out other potential causes of the symptoms – including tumors or strokes.236 Delirium and depression can be common among individuals and are important to rule out.237

Psychological tests for depression are used, since depression can either be concurrent with AD (see Depression of Alzheimer disease), an early sign of cognitive impairment,238 or even the cause.239240

Due to low accuracy, the C-PIB-PET scan is not recommended as an early diagnostic tool or for predicting the development of AD when people show signs of mild cognitive impairment (MCI).241 The use of 18F-FDG PET scans, as a single test, to identify people who may develop Alzheimer's disease is not supported by evidence.242

Prevention

There are no disease-modifying treatments available to cure Alzheimer's disease and because of this, AD research has focused on interventions to prevent the onset and progression.243 There is no evidence that supports any particular measure in preventing AD,244 and studies of measures to prevent the onset or progression have produced inconsistent results. Epidemiological studies have proposed relationships between an individual's likelihood of developing AD and modifiable factors, such as medications, lifestyle, and diet. There are some challenges in determining whether interventions for AD act as a primary prevention method, preventing the disease itself, or a secondary prevention method, identifying the early stages of the disease.245 These challenges include duration of intervention, different stages of disease at which intervention begins, and lack of standardization of inclusion criteria regarding biomarkers specific for AD.246 Further research is needed to determine factors that can help prevent AD.247

Medication

Cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes, and smoking, are associated with a higher risk of onset and worsened course of AD.248249 The use of statins to lower cholesterol may be of benefit in AD.250 Antihypertensive and antidiabetic medications in individuals without overt cognitive impairment may decrease the risk of dementia by influencing cerebrovascular pathology.251252 More research is needed to examine the relationship with AD specifically; clarification of the direct role medications play versus other concurrent lifestyle changes (diet, exercise, smoking) is needed.253

Depression is associated with an increased risk for AD; management with antidepressant medications may provide a preventative measure.254

Historically, long-term usage of non-steroidal anti-inflammatory drugs (NSAIDs) were thought to be associated with a reduced likelihood of developing AD as it reduces inflammation, but NSAIDs do not appear to be useful as a treatment.255 Additionally, because women have a higher incidence of AD than men, it was once thought that estrogen deficiency during menopause was a risk factor, but there is a lack of evidence to show that hormone replacement therapy (HRT) in menopause decreases risk of cognitive decline.256

Lifestyle

Further information: Neurobiological effects of physical exercise

Certain lifestyle activities, such as physical and cognitive exercises, higher education and occupational attainment, cigarette smoking, stress, sleep, and the management of other comorbidities, including diabetes and hypertension, may affect the risk of developing AD.257

Physical exercise is associated with a decreased rate of dementia,258 and is effective in reducing symptom severity in those with AD.259 Memory and cognitive functions can be improved with aerobic exercises including brisk walking three times weekly for forty minutes.260 It may also induce neuroplasticity of the brain.261 Participating in mental exercises, such as reading, crossword puzzles, and chess have shown potential to be preventive.262 Meeting the WHO recommendations for physical activity is associated with a lower risk of AD.263

Higher education and occupational attainment, and participation in leisure activities, contribute to a reduced risk of developing AD,264 or of delaying the onset of symptoms. This is compatible with the cognitive reserve theory, which states that some life experiences result in more efficient neural functioning providing the individual a cognitive reserve that delays the onset of dementia manifestations.265 Education delays the onset of Alzheimer's disease syndrome without changing the duration of the disease.266

Cessation in smoking may reduce risk of developing AD, specifically in those who carry the APOE ɛ4 allele.267268 The increased oxidative stress caused by smoking results in downstream inflammatory or neurodegenerative processes that may increase risk of developing AD.269 Avoidance of smoking, counseling and pharmacotherapies to quit smoking are used, and avoidance of environmental tobacco smoke is recommended.270

Alzheimer's disease is associated with sleep disorders but the precise relationship is unclear.271272 It was once thought that as people get older, the risk of developing sleep disorders and AD independently increase, but research suggests sleep disorders may be a risk factor for AD.273 One theory is that the mechanisms to increase clearance of toxic substances, including Aβ, are active during sleep.274275 With decreased sleep, a person is increasing Aβ production and decreasing Aβ clearance, resulting in Aβ accumulation.276277278 Receiving adequate sleep (approximately 7–8 hours) every night has become a potential lifestyle intervention to prevent the development of AD.279

Stress is a risk factor for the development of AD.280 The mechanism by which stress predisposes someone to development of AD is unclear, but it is suggested that lifetime stressors may affect a person's epigenome, leading to an overexpression or under expression of specific genes.281 Although the relationship of stress and AD is unclear, strategies to reduce stress and relax the mind may be helpful strategies in preventing the progression or Alzheimer's disease.282 Meditation, for instance, is a helpful lifestyle change to support cognition and well-being, though further research is needed to assess long-term effects.283

Management

There is no cure for AD;284 available treatments offer relatively small symptomatic benefits but remain palliative in nature.285286 Treatments can be divided into pharmaceutical, psychosocial, and caregiving.

Pharmaceutical

Medications used to treat the cognitive symptoms of AD rather than the underlying cause include: four acetylcholinesterase inhibitors (tacrine, rivastigmine, galantamine, and donepezil) and memantine, an NMDA receptor antagonist. The acetylcholinesterase inhibitors are intended for those with mild to severe AD, whereas memantine is intended for those with moderate or severe Alzheimer's disease.287 The benefit from their use is small.288289290291

Reduction in the activity of the cholinergic neurons is a well-known feature of AD.292 Acetylcholinesterase inhibitors are employed to reduce the rate at which acetylcholine (ACh) is broken down, thereby increasing the concentration of ACh in the brain and combating the loss of ACh caused by the death of cholinergic neurons.293 There is evidence for the efficacy of these medications in mild to moderate AD,294295 and some evidence for their use in the advanced stage.296 The use of these drugs in mild cognitive impairment has not shown any effect in a delay of the onset of Alzheimer's disease.297 The most common side effects are nausea and vomiting, both of which are linked to cholinergic excess. These side effects arise in approximately 10–20% of users, are mild to moderate in severity, and can be managed by slowly adjusting medication doses.298 Less common secondary effects include muscle cramps, decreased heart rate (bradycardia), decreased appetite and weight, and increased gastric acid production.299

Glutamate is an excitatory neurotransmitter of the nervous system, although excessive amounts in the brain can lead to cell death through a process called excitotoxicity which consists of the overstimulation of glutamate receptors. Excitotoxicity occurs not only in AD, but also in other neurological diseases such as Parkinson's disease and multiple sclerosis.300 Memantine is a noncompetitive NMDA receptor antagonist first used as an anti-influenza agent. It acts on the glutamatergic system by blocking NMDA receptors and inhibiting their overstimulation by glutamate.301302 Memantine has been shown to have a small benefit in the treatment of moderate to severe AD.303 Reported adverse events with memantine are infrequent and mild, including hallucinations, confusion, dizziness, headache and fatigue.304305 The combination of memantine and donepezil306 has been shown to be "of statistically significant but clinically marginal effectiveness".307

An extract of Ginkgo biloba known as EGb 761 has been used for treating AD and other neuropsychiatric disorders.308 Its use is approved throughout Europe.309 The World Federation of Biological Psychiatry guidelines lists EGb 761 with the same weight of evidence (level B) given to acetylcholinesterase inhibitors and memantine. EGb 761 is the only one that showed improvement of symptoms in both AD and vascular dementia. EGb 761 may have a role either on its own or as an add-on if other therapies prove ineffective.310 A 2016 review concluded that the quality of evidence from clinical trials on Ginkgo biloba has been insufficient to warrant its use for treating AD.311

Atypical antipsychotics are modestly useful in reducing aggression and psychosis in people with AD, but their advantages are offset by serious adverse effects, such as stroke, movement difficulties or cognitive decline.312 When used in the long-term, they have been shown to associate with increased mortality.313 They are recommended in dementia only after first line therapies such as behavior modification have failed, and due to the risk of adverse effects, they should be used for the shortest amount of time possible.314 Stopping antipsychotic use in this group of people appears to be safe.315

Psychosocial

Psychosocial interventions are used as an adjunct to pharmaceutical treatment and can be classified within behavior-, emotion-, cognition- or stimulation-oriented approaches.[needs update]316

Behavioral interventions attempt to identify and reduce the antecedents and consequences of problem behaviors. This approach has not shown success in improving overall functioning,317 but can help to reduce some specific problem behaviors, such as incontinence.318 There is a lack of high quality data on the effectiveness of these techniques in other behavior problems such as wandering.319320 Music therapy is effective in reducing behavioral and psychological symptoms.321

Emotion-oriented interventions include reminiscence therapy, validation therapy, supportive psychotherapy, sensory integration, also called snoezelen, and simulated presence therapy. A Cochrane review has found no evidence that this is effective.322 Reminiscence therapy (RT) involves the discussion of past experiences individually or in group, many times with the aid of photographs, household items, music and sound recordings, or other familiar items from the past. A 2018 review of the effectiveness of RT found that effects were inconsistent, small in size and of doubtful clinical significance, and varied by setting.323 Simulated presence therapy (SPT) is based on attachment theories and involves playing a recording with voices of the closest relatives of the person with AD. There is partial evidence indicating that SPT may reduce challenging behaviors.324

The aim of cognition-oriented treatments, which include reality orientation and cognitive retraining, is the reduction of cognitive deficits. Reality orientation consists of the presentation of information about time, place, or person to ease the understanding of the person about its surroundings and his or her place in them. On the other hand, cognitive retraining tries to improve impaired capacities by exercising mental abilities. Both have shown some efficacy improving cognitive capacities.325

Stimulation-oriented treatments include art, music and pet therapies, exercise, and any other kind of recreational activities. Stimulation has modest support for improving behavior, mood, and, to a lesser extent, function. Nevertheless, as important as these effects are, the main support for the use of stimulation therapies is the change in the person's routine.326

Caregiving

Further information: Caring for people with dementia and Palliative care

Since AD has no cure and it gradually renders people incapable of tending to their own needs, caregiving is essentially the treatment and must be carefully managed over the course of the disease.

During the early and moderate stages, modifications to the living environment and lifestyle can increase safety and reduce caretaker burden.327328 Examples of such modifications are the adherence to simplified routines, the placing of safety locks, the labeling of household items to cue the person with the disease or the use of modified daily life objects.329330331 If eating becomes problematic, food will need to be prepared in smaller pieces or even puréed.332 When swallowing difficulties arise, the use of feeding tubes may be required. In such cases, the medical efficacy and ethics of continuing feeding is an important consideration of the caregivers and family members.333334 The use of physical restraints is rarely indicated in any stage of the disease, although there are situations when they are necessary to prevent harm to the person with Alzheimer's disease or their caregivers.335

During the final stages of the disease, treatment is centred on relieving discomfort until death, often with the help of hospice.336

Diet

Diet may be a modifiable risk factor for the development of Alzheimer's disease but more research needs to be conducted.337 The Mediterranean diet, and the DASH diet are both associated with less cognitive decline.338 A different approach has been to incorporate elements of both of these diets into one known as the MIND diet.339 Results from large-scale epidemiological studies and clinical trials have not demonstrated an independent role for most individual dietary components.340

Prognosis

The early stages of AD are difficult to diagnose. A definitive diagnosis is usually made once cognitive impairment compromises daily living activities, although the person may still be living independently. The symptoms will progress from mild cognitive problems, such as memory loss through increasing stages of cognitive and non-cognitive disturbances, eliminating any possibility of independent living, especially in the late stages of the disease.341

Life expectancy of people with AD is reduced.342 The normal life expectancy for 60 to 70 years old is 23 to 15 years; for 90 years old it is 4.5 years.343 Following AD diagnosis it ranges from 7 to 10 years for those in their 60s and early 70s (a loss of 13 to 8 years), to only about 3 years or less (a loss of 1.5 years) for those in their 90s.344

Fewer than 3% of people live more than fourteen years after diagnosis.345 Disease features significantly associated with reduced survival are an increased severity of cognitive impairment, decreased functional level, disturbances in the neurological examination, history of falls, malnutrition, dehydration and weight loss.346 Other coincident diseases such as heart problems, diabetes, or history of alcohol abuse are also related with shortened survival.347348349 While the earlier the age at onset the higher the total survival years, life expectancy is particularly reduced when compared to the healthy population among those who are younger.350 Men have a less favourable survival prognosis than women.[needs update]351352

Aspiration pneumonia is the most frequent immediate cause of death brought by AD.353 While the reasons behind the lower prevalence of cancer in AD patients remain unclear, some researchers hypothesize that biological mechanisms shared by both diseases might play a role. However, this requires further investigation.354

Epidemiology

See also: Alzheimer's disease in African Americans and Alzheimer's Disease in the East Asian Population

Two main measures are used in epidemiological studies: incidence and prevalence. Incidence is the number of new cases per unit of person-time at risk (usually number of new cases per thousand person-years); while prevalence is the total number of cases of the disease in the population at any given time.

Regarding incidence, cohort longitudinal studies (studies where a disease-free population is followed over the years) provide rates between 10 and 15 per thousand person-years for all dementias and 5–8 for AD,355356 which means that half of new dementia cases each year are Alzheimer's disease. Advancing age is a primary risk factor for the disease and incidence rates are not equal for all ages: every 5 years after the age of 65, the risk of acquiring the disease approximately doubles, increasing from 3 to as much as 69 per thousand person years.357358 Females with AD are more common than males, but this difference is likely due to women's longer life spans. When adjusted for age, both sexes are affected by Alzheimer's at equal rates.359 In the United States, the risk of dying from AD in 2010 was 26% higher among the non-Hispanic white population than among the non-Hispanic black population, and the Hispanic population had a 30% lower risk than the non-Hispanic white population.360 However, much AD research remains to be done in minority groups, such as the African American, East Asian and Hispanic/Latino populations.361362 Studies have shown that these groups are underrepresented in clinical trials and do not have the same risk of developing AD when carrying certain genetic risk factors (i.e. APOE4), compared to their caucasian counterparts.363364365

The prevalence of AD in populations is dependent upon factors including incidence and survival. Since the incidence of AD increases with age, prevalence depends on the mean age of the population for which prevalence is given. In the United States in 2020, AD dementia prevalence was estimated to be 5.3% for those in the 60–74 age group, with the rate increasing to 13.8% in the 74–84 group and to 34.6% in those greater than 85.366 Prevalence rates in some less developed regions around the globe are lower.367368 Both the prevalence and incidence rates of AD are steadily increasing, and the prevalence rate is estimated to triple by 2050 reaching 152 million, compared to the 50 million people with AD globally in 2020.[better source needed]369370[better source needed]371

History

The ancient Greek and Roman philosophers and physicians associated old age with increasing dementia.372 It was not until 1901 that German psychiatrist Alois Alzheimer identified the first case of what became known as Alzheimer's disease, named after him, in a fifty-year-old woman he called Auguste D. He followed her case until she died in 1906 when he first reported publicly on it.373 During the next five years, eleven similar cases were reported in the medical literature, some of them already using the term Alzheimer's disease.374 The disease was first described as a distinctive disease by Emil Kraepelin after suppressing some of the clinical (delusions and hallucinations) and pathological features (arteriosclerotic changes) contained in the original report of Auguste D.375 He included Alzheimer's disease, also named presenile dementia by Kraepelin, as a subtype of senile dementia in the eighth edition of his Textbook of Psychiatry, published on 15 July 1910.376

For most of the 20th century, the diagnosis of Alzheimer's disease was reserved for individuals between the ages of 45 and 65 who developed symptoms of dementia. The terminology changed after 1977 when a conference on Alzheimer's disease concluded that the clinical and pathological manifestations of presenile and senile dementia were almost identical, although the authors also added that this did not rule out the possibility that they had different causes.377 This eventually led to the diagnosis of Alzheimer's disease independent of age.378 The term senile dementia of the Alzheimer type (SDAT) was used for a time to describe the condition in those over 65, with classical Alzheimer's disease being used to describe those who were younger. Eventually, the term Alzheimer's disease was formally adopted in medical nomenclature to describe individuals of all ages with a characteristic common symptom pattern, disease course, and neuropathology.379

The National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) and the Alzheimer's Disease and Related Disorders Association (ADRDA, now known as the Alzheimer's Association) established the most commonly used NINCDS-ADRDA Alzheimer's Criteria for diagnosis in 1984,380 extensively updated in 2007.381382 These criteria require that the presence of cognitive impairment, and a suspected dementia syndrome, be confirmed by neuropsychological testing for a clinical diagnosis of possible or probable Alzheimer's disease. A histopathologic confirmation including a microscopic examination of brain tissue is required for a definitive diagnosis. Good statistical reliability and validity have been shown between the diagnostic criteria and definitive histopathological confirmation.383

Society and culture

See also: Alzheimer's disease organizations

Social costs

Dementia, and specifically Alzheimer's disease, may be among the most costly diseases for societies worldwide.384 As populations age, these costs will probably increase and become an important social problem and economic burden.385 Costs associated with AD include direct and indirect medical costs, which vary between countries depending on social care for a person with AD.386387388 Direct costs include doctor visits, hospital care, medical treatments, nursing home care, specialised equipment, and household expenses.389390 Indirect costs include the cost of informal care and the loss in productivity of informal caregivers.391

In the United States as of 2019[update], informal (family) care is estimated to constitute nearly three-fourths of caregiving for people with AD at a cost of US$234 billion per year and approximately 18.5 billion hours of care.392 The cost to society worldwide to care for individuals with AD is projected to increase nearly ten-fold, and reach about US$9.1 trillion by 2050.393

Costs for those with more severe dementia or behavioral disturbances are higher and are related to the additional caregiving time to provide physical care.394

Caregiving burden

Further information: Caregiving and dementia

Individuals with Alzheimer's will require assistance in their lifetime, and care will most likely come in the form of a full-time caregiver which is often a role that is taken on by the spouse or a close relative. Caregiving tends to include physical and emotional burdens as well as time and financial strain at times on the person administering the aid.395396 Alzheimer's disease is known for placing a great burden on caregivers which includes social, psychological, physical, or economic aspects.397398399 Home care is usually preferred by both those people with Alzheimer's disease as well as their families.400 This option also delays or eliminates the need for more professional and costly levels of care.401402 Nevertheless, two-thirds of nursing home residents have dementias.403

Dementia caregivers are subject to high rates of physical and mental disorders.404 Factors associated with greater psychosocial problems of the primary caregivers include having an affected person at home, the caregiver being a spouse, demanding behaviors of the cared person such as depression, behavioral disturbances, hallucinations, sleep problems or walking disruptions and social isolation.405406 In the United States, the yearly cost of caring for a person with dementia ranges from $28,078-$56,022 per year for formal medical care and $36,667-$92,689 for informal care provided by a relative or friend (assuming market value replacement costs for the care provided by the informal caregiver) and $15,792-$71,813 in lost wages.407

Cognitive behavioral therapy and the teaching of coping strategies either individually or in group have demonstrated their efficacy in improving caregivers' psychological health.408409

Media

Main article: Alzheimer's disease in the media

Alzheimer's disease has been portrayed in films such as: Iris (2001), based on John Bayley's memoir of his wife Iris Murdoch;410 The Notebook (2004), based on Nicholas Sparks's 1996 novel of the same name;411 A Moment to Remember (2004); Thanmathra (2005);412 Memories of Tomorrow (Ashita no Kioku) (2006), based on Hiroshi Ogiwara's novel of the same name;413 Away from Her (2006), based on Alice Munro's short story The Bear Came over the Mountain;414 Still Alice (2014), about a Columbia University professor who has early onset Alzheimer's disease, based on Lisa Genova's 2007 novel of the same name and featuring Julianne Moore in the title role. Documentaries on Alzheimer's disease include Malcolm and Barbara: A Love Story (1999) and Malcolm and Barbara: Love's Farewell (2007), both featuring Malcolm Pointon.415416417

Alzheimer's disease has also been portrayed in music by English musician the Caretaker in releases such as Persistent Repetition of Phrases (2008), An Empty Bliss Beyond This World (2011), and Everywhere at the End of Time (2016–2019).418419420 Paintings depicting the disorder include the late works by American artist William Utermohlen, who drew self-portraits from 1995 to 2000 as an experiment of showing his disease through art.421422

Research directions

See also: Anti-amyloid drugs

Antibodies may have the ability to alter the disease course by targeting amyloid beta with immunotherapy medications such as donanemab and lecanemab.423424425

Lecanemab was approved via the FDA accelerated approval process,426427428429 and was converted to traditional approval in July 2023, after further testing, along with the addition of a boxed warning about amyloid-related imaging abnormalities.430431 As of early August 2024, lecanemab was approved for sale in Japan, South Korea, China, Hong Kong and Israel although it was recommended against approval by an advisory body of the European Union on July 26, citing its side effects.432

Donanemab was approved by the FDA in July 2024.433 Anti-amyloid drugs also cause brain shrinkage.434 The cholinesterase inhibitor benzgalantamine was approved by the FDA in July 2024.435

Specific medications that may reduce the risk or progression of Alzheimer's disease have been studied.436 The research trials investigating medications generally impact Aβ plaques, inflammation, APOE, neurotransmitter receptors, neurogenesis, growth factors or hormones.437438439

Machine learning algorithms with electronic health records are being studied as a way to predict Alzheimer's disease earlier.440

Wikimedia Commons has media related to Alzheimer's disease. Look up Alzheimer's disease in Wiktionary, the free dictionary.

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