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Alzheimer's disease ( AD) is a neurodegenerative disease and the cause of 60–70% of cases of . The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include , disorientation (including easily getting lost), , loss of , , and behavioral issues. As a person's condition declines, they often . Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the average life expectancy following diagnosis is three to twelve years.

The causes of Alzheimer's disease remain poorly understood. There are many environmental and genetic associated with its development. The strongest genetic risk factor is from an of . Other risk factors include a history of , clinical depression, and high blood pressure. The progression of the disease is largely characterised by the accumulation of in the , called and neurofibrillary tangles. These misfolded protein aggregates interfere with normal cell function, and over time lead to irreversible degeneration of neurons and loss of in the . A probable diagnosis is based on the history of the illness and , with and to rule out other possible causes. Initial symptoms are often mistaken for normal brain aging. is needed for a definite diagnosis, but this can only take place after death.

No treatments can stop or reverse its progression, though some may temporarily improve symptoms. A , physical activity, and social engagement are generally beneficial in aging, and may help in reducing the risk of cognitive decline and Alzheimer's. Affected people become increasingly reliant on others for assistance, often placing a burden on caregivers. The pressures can include social, psychological, physical, and economic elements. Exercise programs may be beneficial with respect to activities of daily living and can potentially improve outcomes. Behavioral problems or due to dementia are sometimes treated with , but this has an increased risk of early death.

As of 2020, there were approximately 50 million people worldwide with Alzheimer's disease. It most often begins in people over 65 years of age, although up to 10% of cases are early-onset impacting those in their 30s to mid-60s. It affects about 6% of people 65 years and older, and women more often than men. The disease is named after German psychiatrist and pathologist , who first described it in 1906. Alzheimer's financial burden on society is large, with an estimated global annual cost of trillion. It is ranked as the seventh leading cause of death worldwide.

Given the widespread impacts of Alzheimer's disease, both basic-science and health funders in many countries support Alzheimer's research at large scales. For example, the US National Institutes of Health program for Alzheimer's research, the National Plan to Address Alzheimer's Disease, has a budget of US$3.98 billion for fiscal year 2026. In the , the 2020 research programme awarded over €570 million for dementia-related projects.

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

First symptoms
The first symptoms are often mistakenly attributed to or stress. 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. These early symptoms can affect the most complex activities of daily living. 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.

Subtle problems with the executive functions of , , flexibility, and , or impairments in (memory of meanings, and concept relationships) can also be symptomatic of the early stages of Alzheimer's disease. and depression can be seen at this stage, with apathy remaining as the most persistent symptom throughout the course of the disease.

(2025). 9780444640123, Elsevier.
(2025). 9781437704341, Elsevier/Saunders.
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 and is frequently seen as a or early stage of Alzheimer's disease. Amnestic MCI has a greater than 90% likelihood of being associated with Alzheimer's.

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, (), or execution of movements () are more prominent than memory problems. Alzheimer's disease does not affect all memory capacities equally. of the person's life (), facts learned (), and (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.

Language problems are mainly characterised by a shrinking and decreased word , leading to a general impoverishment of oral and . In this stage, the person with Alzheimer's is usually capable of communicating basic ideas adequately. While performing fine motor tasks such as writing, drawing, or dressing, certain movement coordination and planning difficulties () may be present; however, they are commonly unnoticed. 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.

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

Behavioral and changes become more prevalent. Common manifestations are wandering, and emotional lability, leading to crying, outbursts of unpremeditated , or resistance to caregiving. can also appear. Approximately 30% of people with Alzheimer's disease develop illusionary misidentifications and other symptoms. Subjects also lose insight of their disease process and limitations (). Urinary incontinence can develop. These symptoms create stress for relatives and caregivers, which can be reduced by moving the person from to other .

Late stage
During the final stage, known as the late-stage or severe stage, there is complete dependence on caregivers. Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech. Despite the loss of verbal language abilities, people can often understand and return emotional signals. Although aggressiveness can still be present, extreme and exhaustion are much more common symptoms. People with Alzheimer's disease will ultimately not be able to perform even the simplest tasks independently; 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 or , not the disease itself. In some cases, there is a paradoxical lucidity immediately before death, where there is an unexpected recovery of mental clarity.

Causes
Alzheimer's disease is believed to occur when abnormal amounts of (Aβ), accumulating extracellularly as and , or intracellularly as neurofibrillary tangles, form in the brain, affecting neuronal functioning and connectivity, resulting in a progressive loss of brain function. This altered is age-related, regulated by brain cholesterol, and associated with other neurodegenerative diseases.
(2025). 9780199638499, Oxford University Press.

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

Genetic
Late onset
Late-onset Alzheimer's is about 70% . Most cases of Alzheimer's are not familial, and so they are termed sporadic Alzheimer's disease. Of the cases of sporadic Alzheimer's disease, most are classified as late onset where they are developed after the age of 65 years.

The strongest genetic risk factor for sporadic Alzheimer's disease is APOEε4. APOEε4 is one of four alleles of (APOE). APOE plays a major role in lipid-binding proteins in lipoprotein particles and the ε4 allele disrupts this function. Between 40% and 80% of people with Alzheimer's disease possess at least one APOEε4 allele. The APOEε4 allele increases the risk of the disease by three times in and by 15 times in . Like many human diseases, environmental effects and genetic modifiers result in incomplete . For example, Nigerian 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.

Early onset
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. Less than 5% of sporadic Alzheimer's disease have an earlier onset, and early-onset Alzheimer's is about 90% heritable. Familial Alzheimer's disease usually implies two or more persons affected in one or more generations.

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

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

A Japanese pedigree of familial Alzheimer's disease was found to be associated with a deletion mutation of codon 693 of APP. This mutation and its association with Alzheimer's disease was first reported in 2008, 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.

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

Misfolded amyloid beta and tau proteins are associated with the disease, bringing about that leads to neuroinflammation. This chronic inflammation is a feature of other neurodegenerative diseases including Parkinson's disease, and .

Infection
Spirochete infections have been linked to dementia.

DNA damage
DNA damages accumulate in affected brains; reactive oxygen species may be the major source of this DNA damage.

Amyloid
The amyloid hypothesis claimed that extracellular amyloid beta (Aβ) deposits are the fundamental cause. Support 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 () who have an extra almost universally exhibit at least early symptoms by age 40. A specific of , APOE4, is a major genetic risk factor. While apolipoproteins enhance the breakdown of amyloid beta, some isoforms are less effective at this task (such as APOE4), leading to amyloid buildup in the brain.

Cholinergic
The cholinergic hypothesis proposed that reduced synthesis of the neurotransmitter was involved. The loss of cholinergic neurons in the and cerebral cortex is a key feature.

Sleep
Sleep disturbances are seen as a possible for inflammation in Alzheimer's disease. Sleep disruption was previously only seen as a consequence of Alzheimer's disease, but , accumulating evidence suggests that this relationship may be .

Metal toxicity, smoking, neuroinflammation and air pollution
The cellular 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. Smoking is a significant Alzheimer's disease risk factor. Systemic markers of the innate immune system are risk factors for late-onset Alzheimer's disease. Exposure to air pollution may be a contributing factor to the development of Alzheimer's disease.

Age-related myelin decline
Retrogenesis is a medical that just as the fetus goes through a process of beginning with and ending with , the brains of people with Alzheimer's disease go through a reverse neurodegeneration process starting with and death of axons (white matter) and ending with the death of grey matter. 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.

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

Other hypotheses
The association with 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.

Studies have reported a potential link between infection with certain viruses and developing Alzheimer's disease later in life. Notably, a large scale study conducted on 6,245,282 patients has reported an increased risk of developing Alzheimer's disease following COVID-19 infection in cognitively normal individuals over 65.

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.

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.

Pathophysiology
Neuropathology
Alzheimer's disease is characterised by loss of and in the and certain subcortical regions. This loss results in gross of the affected regions, including degeneration in the and , and parts of the and . Degeneration is also present in nuclei particularly the in the . 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.

Both Aβ and neurofibrillary tangles are clearly visible by in brains of those with Alzheimer's disease, especially in the . However, Alzheimer's disease may occur without neurofibrillary tangles in the . Plaques are dense, mostly deposits of peptide and cellular material outside and around . Neurofibrillary tangles are aggregates of the microtubule-associated 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 . are not rare in the brains of people with Alzheimer's disease.

Biochemistry
Amyloid beta
Alzheimer's disease has been identified as a protein misfolding disease, a , caused by the accumulation of abnormally folded protein into amyloid plaques, and tau protein into neurofibrillary tangles in the brain. Plaques are made up of small , 39–43  in length, called amyloid beta. Amyloid beta is a fragment from the larger amyloid-beta precursor protein (APP) a transmembrane protein that penetrates the . APP is critical to neuron growth, survival, and post-injury repair. In Alzheimer's disease, and beta secretase act together in a process which causes APP to be divided into smaller fragments. 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 of amyloid beta, which then form clumps that deposit outside neurons in dense formations known as amyloid plaques. Excitatory neurons are known to be the major producers of amyloid beta that contribute to major extracellular plaque deposition.

Phosphorylated tau
Alzheimer's disease is also considered a due to abnormal aggregation of the . Every neuron has a , an internal support structure partly made up of structures called . These microtubules act like tracks, guiding nutrients and molecules from the body of the cell to the ends of the and back. A protein called tau stabilises the microtubules when , 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. Pathogenic tau can also cause neuronal death through transposable element dysregulation. has also been reported as a mechanism of cell death in brain cells affected with tau tangles.Balusu S, Horré K, Thrupp N, Craessaerts K, Snellinx A, Serneels L, T'Syen D, Chrysidou I, Arranz AM, Sierksma A, Simrén J, Karikari TK, Zetterberg H, Chen WT, Thal DR, Salta E, Fiers M, De Strooper B. MEG3 activates necroptosis in human neuron xenografts modeling Alzheimer's disease. Science. 2023 Sep 15;381(6663):1176-1182.

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

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, and the beneficial effect of therapeutics (such as monoclonal antibodies) promoting Aβ clearance has ranged from nonexistent to modest.

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

Various inflammatory processes and may also have a role in the pathology of Alzheimer's disease. 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. 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.

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.

Evidence has accrued for as central actors in the mechanism of AD. Microglia are topographically associated with pTau and Aβ within the brain, even when each pathologic component occurs in distinct brain regions, 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. Microglia are the principal immunological cells of the central nervous system, serving as the 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. However, microglia can also be a major source of pro-inflammatory mediators which can be deleterious to neurological function.

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. 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.

AD is usually clinically diagnosed based on a person's , observations from friends or relatives, and behavioral changes. The presence of characteristic 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, 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. Advanced 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.

(2025). 9781846293122, (UK) National Institute for Health and Clinical Excellence. .
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). FDG-PET scan is not required for the diagnosis but it is sometimes used when standard testing is unclear. FDG-PET shows a bilateral, asymmetric, temporal and parietal reduced activity. Advanced imaging may predict conversion from stages (mild cognitive impairment) to Alzheimer's disease. FDA-approved radiopharmaceutical diagnostic agents used in PET for Alzheimer's disease are (2012), (2013), (2014), and flortaucipir (2020). Because many insurance companies in the United States do not cover this procedure, its use in clinical practice is largely limited to clinical trials .

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

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.

Eight intellectual domains are most commonly impaired in AD—, , , , , orientation, and executive functional abilities, as listed in the fourth text revision of the DSM (DSM-IV-TR).

(2025). 9780890420256, American Psychiatric Association.

The DSM-5 defines criteria for probable or possible AD for both major and mild neurocognitive disorder.

(2025). 9780890425558, American Psychiatric Association.
Major or mild neurocognitive disorder must be present along with at least one cognitive deficit for a diagnosis of either probable or possible AD. For major neurocognitive disorder due to AD, probable Alzheimer's disease can be diagnosed if the individual has genetic evidence of AD
(2025). 9780203772287, Routledge.
or if two or more acquired cognitive deficits, and a functional disability that is not from another disorder, are present. Otherwise, possible AD can be diagnosed as the diagnosis follows an atypical route. 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.

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

Techniques
Neuropsychological tests including 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.
(2025). 9781260469868, McGraw Hill.
These tests may not always be accurate, as they lack sensitivity to mild cognitive impairment, and can be biased by language or attention problems; more comprehensive test arrays are necessary for high reliability of results, particularly in the earliest stages of the disease.

Further neurological examinations are crucial in the differential diagnosis of Alzheimer's disease and other diseases. 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 . A caregiver's viewpoint is particularly important, since a person with Alzheimer's disease is commonly . Many times, families have difficulties in the detection of initial dementia symptoms and may not communicate accurate information to a physician.

Supplemental testing can rule out other potentially treatable diagnoses and help avoid misdiagnoses.

(2025). 9781260121117, McGraw-Hill Medical.
Common supplemental tests include , thyroid function tests, as well as tests to assess vitamin B12 levels, rule out and rule out metabolic problems (including tests for kidney function, electrolyte levels and for ). MRI or CT scans might also be used to rule out other potential causes of the symptoms – including tumors or strokes. and depression can be common among individuals and are important to rule out.
(2025). 9783030567392, Springer.

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, or even the cause.

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). 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.

In May 2025, the US FDA approved a blood test by Fujirebio Diagnostics’ Lumipulse G pTau217/ß-Amyloid 1-42 Plasma Ratio diagnostic device for the early detection of amyloid plaques associated with AD in adults aged 55 years and older who are exhibiting signs and symptoms of the disease.

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. There is no evidence that supports any particular measure in preventing AD, 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. 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. Further research is needed to determine factors that can help prevent AD.

Medication
Cardiovascular risk factors, such as hypercholesterolaemia, , , and , are associated with a higher risk of onset and worsened course of AD. The use of to lower may be of benefit in AD. Antihypertensive and antidiabetic medications in individuals without overt cognitive impairment may decrease the risk of dementia by influencing cerebrovascular . 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.

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

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. Additionally, because women have a higher incidence of AD than men, it was once thought that estrogen deficiency during 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.

Lifestyle
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.

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

Higher education and occupational attainment, and participation in leisure activities, contribute to a reduced risk of developing AD, 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. delays the onset of Alzheimer's disease syndrome without changing the duration of the disease.

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

Alzheimer's disease is associated with but the precise relationship is unclear. 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. One theory is that the mechanisms to increase clearance of toxic substances, including , are active during sleep. With decreased sleep, a person is increasing Aβ production and decreasing Aβ clearance, resulting in Aβ accumulation. Receiving adequate sleep (approximately 7–8 hours) every night has become a potential lifestyle intervention to prevent the development of AD.

Stress is a risk factor for the development of AD. 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 , leading to an overexpression or under expression of specific genes. 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. Meditation, for instance, is a helpful lifestyle change to support cognition and well-being, though further research is needed to assess long-term effects.

Management
There is no cure for AD; available treatments offer relatively small symptomatic benefits but remain in nature.
(2025). 9781496387394, Wolters Kluwer.
Treatments can be divided into pharmaceutical, psychosocial, and caregiving.

Pharmaceutical
Symptomatic treatment
Medications used to treat the cognitive symptoms of AD rather than the underlying cause include: four acetylcholinesterase inhibitors (, , , and ) and , 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. The benefit from their use is small.
(2025). 9781259834400, McGraw Hill.

Reduction in the activity of the neurons is a well-known feature of AD. Acetylcholinesterase inhibitors are employed to reduce the rate at which the body breaks down (ACh), thereby increasing the concentration of ACh in the brain and combating the loss of ACh caused by the death of cholinergic neurons. Evidence supports medical efficacy in mild to moderate AD, and somewhat in the advanced stage. This does not extend to delaying symptom onset.

Glutamate is an excitatory , although in excess can lead to cell death through a process called which consists of the overstimulation of glutamate receptors. Excitotoxicity also occurs in other neurological diseases such as Parkinson's disease and multiple sclerosis.

is a noncompetitive NMDA receptor antagonist first used as an anti- agent. It acts on the glutamatergic system by blocking and inhibiting their overstimulation by glutamate. Memantine has been reported to have a small benefit in the treatment of moderate to severe AD. The combination of memantine and donepezil has been reported to be "of statistically significant but clinically marginal effectiveness".

An extract of known as EGb 761 has been used for treating AD and other neuropsychiatric disorders. Its use is approved throughout Europe. 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 to other therapies. A 2016 review concluded that the quality of evidence from clinical trials on G. biloba has been insufficient to warrant its use.

Atypical antipsychotics are modestly useful in reducing and in people with AD, but their advantages are offset by serious adverse effects, such as , movement difficulties or cognitive decline. When used in the long-term, they have been reported to associate with increased mortality. See Https://medicalxpress.com/news/2009-01-antipsychotic-drugs-death-alzheimer-patients.html" target="_blank" rel="nofollow"> lay summary, January 2009. 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. Stopping antipsychotic use in this group of people appears to be safe.

is a cholinesterase inhibitor.

Side effects
The most common side effects are and , 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.
(2025). 9781609137137, Wolters Kluwer Health/Lippincott Williams & Wilkins.
Less common secondary effects include muscle , decreased (), decreased and weight, and increased production. Reported adverse events with memantine are infrequent and mild, including , , , and .

Antibodies
Two have been approved to target amyloid beta: and .

Lecanemab is approved in the US, including a about amyloid-related imaging abnormalities. As of early August 2024, lecanemab was approved for sale in , , , and although not by an advisory body of the European Union on July 26, citing side effects.

is approved in the US.

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

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

Emotion-oriented interventions include reminiscence therapy, validation therapy, supportive , sensory integration, also called , and simulated presence therapy. A Cochrane review has found no evidence that this is effective. 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. 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.

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 reported some efficacy improving cognitive capacities.

Stimulation-oriented treatments include , music and pet therapies, , 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.

Caregiving
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 and reduce caretaker burden. 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. If eating becomes problematic, food will need to be prepared in smaller pieces or even puréed.

(2025). 9780781766517, Lippincott Williams & Wilkins. .
When arise, the use of may be required. In such cases, the medical efficacy and ethics of continuing feeding is an important consideration of the caregivers and family members. 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.

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

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

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.

of people with AD is reduced. The normal life expectancy for 60 to 70 years old is 23 to 15 years; for 90 years old it is 4.5 years. 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.

Fewer than 3% of people live more than fourteen years after diagnosis. 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, , and . Other coincident diseases such as heart problems, diabetes, or history of are also related with shortened survival. 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. Men have a less favourable survival prognosis than women.

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

Epidemiology
Two main measures are used in 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 is the total number of cases of the disease in the population at any given time. [[File:Alzheimer's disease and other dementias world map-Deaths per million persons-WHO2012.svg|thumb|upright=1.35|Deaths per million persons in 2012 due to dementias including Alzheimer's disease

]]

Regarding incidence, 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, 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. 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.

(2025). 9781259861734, McGraw Hill.
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.Tejada-Vera B. (2013). Mortality from Alzheimer's Disease in the United States: Data for 2000 and 2010. Hyattsville, MD: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics. However, much AD research remains to be done in minority groups, such as the African American, East Asian and Hispanic/Latino populations. Studies have reported 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.

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. Prevalence rates in some less developed regions around the globe are lower. 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.

History
The ancient Greek and Roman philosophers and associated old age with increasing . It was not until 1901 that German psychiatrist identified the first case of what became known as Alzheimer's disease, named after him, in a fifty-year-old woman he called . He followed her case until she died in 1906 when he first reported publicly on it.Auguste D.:
  • (2025). 9780231118965, Columbia University Press. .
    During the next five years, eleven similar cases were reported in the medical literature, some of them already using the term Alzheimer's disease. The disease was first described as a distinctive disease by after suppressing some of the clinical (delusions and hallucinations) and pathological features (arteriosclerotic changes) contained in the original report of Auguste D. He included Alzheimer's disease, also named presenile by Kraepelin, as a subtype of senile dementia in the eighth edition of his Textbook of Psychiatry, published on 15 July 1910.
    (2025). 9781432508333, Kessinger Publishing.

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 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.

(1978). 9780890042250, Raven Press.
This eventually led to the diagnosis of Alzheimer's disease independent of age. 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 to describe individuals of all ages with a characteristic common symptom pattern, disease course, and .

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, extensively updated in 2007. 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 confirmation including a examination of is required for a definitive diagnosis. Good statistical reliability and validity have been reported between the diagnostic criteria and definitive histopathological confirmation.

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

In the United States , 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. 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.

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

Caregiving burden
Individuals with Alzheimer's will require assistance in their lifetime, and care will most likely come in the form of a full-time 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. Alzheimer's disease is known for placing a great burden on caregivers which includes social, psychological, physical, or economic aspects. Home care is usually preferred by both those people with Alzheimer's disease as well as their families. This option also delays or eliminates the need for more professional and costly levels of care. Nevertheless, two-thirds of nursing home residents have dementias.

Dementia caregivers are subject to high rates of physical and disorders. 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 . 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.

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

Media
Alzheimer's disease has been portrayed in films such as: Iris (2001), based on John Bayley's memoir of his wife ;
(2025). 9780349112152, Abacus.
The Notebook (2004), based on 's 1996 novel of the same name;
(1996). 9780786208210, Thorndike Press. .
A Moment to Remember (2004); (2005); Memories of Tomorrow (Ashita no Kioku) (2006), based on Hiroshi Ogiwara's novel of the same name;
(2025). 9784334924461, Kōbunsha.
Away from Her (2006), based on 's The Bear Came over the Mountain;
(2025). 9780375413001, A.A. Knopf.
(2014), about a Columbia University professor who has early onset Alzheimer's disease, based on 's 2007 novel of the same name and featuring 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 .

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 (20162019). 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.

Research
Specific medications that may reduce the risk or progression of Alzheimer's disease include those that impact Aβ , inflammation, , neurotransmitter receptors, neurogenesis, or hormones.

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

Between 1995 and 2021, more than 140 clinical trials costing $42.5B yielded no drugs. As of 2025, 182 clinical trials were testing 138 drugs against multiple targets.

External links
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