Alzheimer's – a Disease makes History
In over 100 years, Alzheimer's disease has developed from a marginal phenomenon into a global social problem. Many possible risk factors are now known. However, there is still no cure.
Scientific support: Prof. Dr. Anja Schneider
Published: 20.10.2025
Difficulty: easy
- Alois Alzheimer described the disease in 1907 based on the case of a patient named Auguste Deter in Frankfurt am Main. In 1910, it was mentioned for the first time under the name Alzheimer's disease. Alzheimer's disease is a neurodegenerative disorder and a form of dementia. In addition to Alzheimer's, there are other types of dementia, such as Frontotemporal dementia and vascular dementia.
- Alzheimer's is the most common form of dementia in people over the age of 60, accounting for about 60 percent of all dementia cases.
- Alzheimer's is defined by the presence of deposits in the brain: so-called Beta-amyloid Plaques between the cells and thread-like tau fibrils in the nerve cells.
- Alzheimer's is a multifactorial disease, meaning there are numerous causes and risk factors, including genetic and epigenetic influences, lifestyle, and certain pre-existing conditions.
- The most important proven risk factor is old age.
- Until recently, there was no causal treatment; only the symptoms could be alleviated with medication. Although the latest drugs are effective against amyloid plaques and slow down the progression of the disease, they cannot yet cure it.
Alzheimer's disease
Morbus Alzheimer
Alzheimer's disease is a progressive neurodegenerative disorder characterized by cortical atrophy, nerve cell loss, synapse loss, and deposits of amyloid plaques and neurofibrillary tangles, leading to dementia and loss of function. Early symptoms include memory problems, speech disorders, executive deficits, depressive moods, and subtle personality changes. As the disease progresses, global cognitive impairment, aphasia, agnosia, apraxia, and behavioral abnormalities such as apathy, restlessness, and sleep disorders occur. The disease was first described in 1907 by Alois Alzheimer.
dementia
Dementia
Dementia is an acquired deficit of cognitive, social, motor, and emotional abilities. The most well-known form is Alzheimer's disease. "De mentia" means "without mind" in English.
Frontotemporal dementia
Pick's disease
Frontotemporal dementia is a neurodegenerative disease. Unlike Alzheimer's dementia, Pick's disease usually begins before the age of 60 and initially manifests itself through changes in personality and social behavior. There are also variants that begin with speech disorders. In advanced stages, memory performance is also impaired. The physiological cause is degeneration of nerve cells in the frontal and temporal lobes of the brain. Similar to Alzheimer's disease, the aggregation of certain proteins appears to play a role in pathogenesis. However, doctors do not yet understand exactly what happens in this process and what other factors contribute to the development of Pick's disease. Today, classic Pick's disease is only a subtype of FTD in which characteristic Pick bodies can be detected in the brain.
vascular
The term refers to vessels in the body in which fluids such as blood or lymph circulate. In a narrower sense, doctors refer to the network of veins, arteries, and capillaries as the "vascular system." If the vascular system is blocked, for example as a result of a stroke, less blood reaches the brain. This means that it receives less oxygen and other nutrients. This can lead to impaired cognitive functions and the development of "vascular dementia." After degenerative forms of dementia such as Alzheimer's, vascular dementia is the second most common form of this group of diseases.
Beta-amyloid
A peptide consisting of 36 to 42 amino acids that is considered the main component of senile plaques and is believed to be responsible for the development of Alzheimer's disease. The starting product is the amyloid precursor protein (APP). Certain enzymes in the cell membrane cut the precursor protein into peptides of various sizes. Amyloids consisting of 40 and 42 amino acids are found in senile plaques, with the 42-amino-acid product forming aggregates particularly quickly, at least in the Petri dish. The normal function of beta-amyloid has not yet been conclusively clarified.
Plaques
Senile plaques
Senile plaques accumulate in the gray matter of the brain when a protein – known as amyloid precursor protein – is not broken down correctly. Inflammation and disorders of fat or sugar metabolism can promote plaque formation. On average, the deposits reach a diameter of 50 micrometers. The appearance of plaques is one of several anatomical changes in the brain that pathologists can use to diagnose Alzheimer's disease after death.
- The global cost of Alzheimer's and other dementias was estimated at approximately $1.3 trillion for 2019.
- About three-quarters of the costs are incurred in high-income countries, mainly North America and Western Europe.
- In some high-income countries, between one-third and one-half of people with dementia are placed in costly residential and nursing homes. The annual cost there is $45,500 per patient.
- In low-income countries, only a small proportion of people with dementia live in nursing homes. There, unpaid, informal care is usually provided by relatives and other caregivers. As a result, the average annual cost is “only” $2,575.
- The costs of informal and formal care each account for about 42 percent of Alzheimer's-related costs, while the direct costs of medical therapies are much lower.
- Low-income countries recently accounted for only about 0.25 percent of global costs, while these countries account for 2.5 percent of global cases. Middle-income countries, on the other hand, accounted for about 25 percent of global costs (with 60 percent of cases), while high-income countries accounted for 74 percent of costs and 39 percent of all patients. However, poorer countries are catching up, with strong growth reported particularly in Africa.
- It is estimated that global costs will rise by about 5 percent annually and reach approximately $1.6 trillion in 2050.
dementia
Dementia
Dementia is an acquired deficit of cognitive, social, motor, and emotional abilities. The most well-known form is Alzheimer's disease. "De mentia" means "without mind" in English.
- According to statistics, 35.6 million people suffered from dementia in 2010. It is estimated that 24 million of them had not yet been diagnosed.
- In 2019, the figure was 57 million.
- According to the Global Burden of Disease Study 2019, the number of patients is expected to rise to 152.8 million by 2050. This is mainly due to the growing population and the higher average age of the population. In contrast, the proportion of people with the disease in the various age groups will remain relatively unchanged.
- Broken down by region, the increase in patients will be lowest in the rich countries of the Pacific region (+53%), followed by Western Europe (+74%). In North Africa, the Middle East, and the eastern part of the sub-Saharan countries, however, researchers from the Global Burden of Disease Study expect the number of cases to increase sevenfold (approx. 350% in each case).
dementia
Dementia
Dementia is an acquired deficit of cognitive, social, motor, and emotional abilities. The most well-known form is Alzheimer's disease. "De mentia" means "without mind" in English.
The history of Alzheimer's disease began in 1901 with the admission of Auguste Deter to the “Institution for the Insane and Epileptics” in Frankfurt am Main. The patient suffered from forgetfulness and delusions. The transcript of the conversation that the psychiatrist in charge subsequently made wrote scientific history.
It marked the beginning of research into a disease that entered medical history under the name of the psychiatrist: Alois Alzheimer ▸ Alois Alzheimer – Neurologist with a Microscope. The preliminary diagnosis was “presenile insanity.”
Alzheimer's disease
Morbus Alzheimer
Alzheimer's disease is a progressive neurodegenerative disorder characterized by cortical atrophy, nerve cell loss, synapse loss, and deposits of amyloid plaques and neurofibrillary tangles, leading to dementia and loss of function. Early symptoms include memory problems, speech disorders, executive deficits, depressive moods, and subtle personality changes. As the disease progresses, global cognitive impairment, aphasia, agnosia, apraxia, and behavioral abnormalities such as apathy, restlessness, and sleep disorders occur. The disease was first described in 1907 by Alois Alzheimer.
Different types of dementia and their causes
The term dementia describes a syndrome, a combination of several signs of illness (symptoms). These include cognitive deficits, deficits in word finding, and later in orientation and everyday skills. The causes of these symptoms remained unknown during Auguste Deter's lifetime; only their effects could be recorded. The dementia later named after Alzheimer initially manifests as Short-term memory impairment. Over time, Long-term memory also disappears, causing those affected to lose more and more abilities and skills until they are no longer able to cope with everyday life.
Today, we know that there are several types of dementia and that there are many possible causes. Alzheimer's dementia, along with frontotemporal dementia, Lewy body dementia, and Parkinson's dementia, is one of the neurodegenerative diseases in which nerve cells are destroyed. However, vascular (blood vessel-related) dementias are also common. In addition, there are secondary forms of dementia that can be the result of Multiple sclerosis or a metabolic disorder, for example.
dementia
Dementia
Dementia is an acquired deficit of cognitive, social, motor, and emotional abilities. The most well-known form is Alzheimer's disease. "De mentia" means "without mind" in English.
Short-term memory
Short-term memory is a type of temporary storage in the brain where information can be retained for a few seconds to a few minutes. Its capacity is very limited, at 7±2 units of information (chunks). These can be numbers, letters, or words, for example. Today, this memory is usually considered within the framework of the working memory model, which also emphasizes the active processing of content.
Long-term memory
Long-term memory stores information about events, facts, or skills over long periods of time, often for a lifetime. Different types of memory are stored in different areas of the brain. The cellular basis for these learning processes is based, among other things, on improved communication between two cells and is called long-term potentiation.
vascular
The term refers to vessels in the body in which fluids such as blood or lymph circulate. In a narrower sense, doctors refer to the network of veins, arteries, and capillaries as the "vascular system." If the vascular system is blocked, for example as a result of a stroke, less blood reaches the brain. This means that it receives less oxygen and other nutrients. This can lead to impaired cognitive functions and the development of "vascular dementia." After degenerative forms of dementia such as Alzheimer's, vascular dementia is the second most common form of this group of diseases.
Multiple sclerosis
encephalomyelitis disseminata
A common neurological disease that predominantly occurs in young adults. For reasons that are still unclear, the body's own cells attack and destroy the myelin sheaths of nerve cells. This can happen throughout the central nervous system, which is why two different multiple sclerosis patients can suffer from very different symptoms. Common symptoms include visual disturbances, numbness in the arms and legs, but also coordination problems, muscle weakness, and bladder problems.
1903–1910: Organic causes?
When Alzheimer moved to Munich in 1903, there was still no classification of mental disorders. Furthermore, the organic causes of mental illness were still far from being generally accepted. From 1903 to 1906, Auguste Deter remained in the Frankfurt institution, but Alzheimer monitored her condition, which was deteriorating, from afar. She died in 1906, “completely demented,” as Alzheimer noted.
When he examined Deter's brain under a microscope, he found destroyed nerve cells with bundles of fibrous structures – Neurofibrils – as well as deposits outside the cells, known as senile Plaques. For Alzheimer, this confirmed his theory that mental illnesses must have organic causes. In 1907, he published a treatise “on a peculiar disease of the cerebral cortex,” but it was not until later that the opinion prevailed that Deter had suffered from a new type of disease. In 1910, the Lehrbuch der Psychiatrie (Textbook of Psychiatry) listed this form for the first time under the name “Alzheimer's disease.”
Neurofibrils
Neurofibrils are fine fibrous structures in nerve cells that consist mainly of neurofilaments (a form of intermediate filaments) and other components of the cytoskeleton. They run in bundles through the cell body and the extensions of neurons and contribute significantly to the stabilization and shaping of the nerve cell. They appear as characteristic features of neurons even in the early embryo.
Alzheimer's disease causes profound changes in cytoskeletal structures: the protein tau, which normally stabilizes microtubules, becomes excessively phosphorylated, detaches from the microtubules, and aggregates to form the typical neurofibrillary tangles (fibrillary bundles). These are a central pathological feature of the disease.
Plaques
Senile plaques
Senile plaques accumulate in the gray matter of the brain when a protein – known as amyloid precursor protein – is not broken down correctly. Inflammation and disorders of fat or sugar metabolism can promote plaque formation. On average, the deposits reach a diameter of 50 micrometers. The appearance of plaques is one of several anatomical changes in the brain that pathologists can use to diagnose Alzheimer's disease after death.
The 1970s and 1980s: First initiatives, first controversy
Until the early 1970s, the mechanisms remained unclear, but it became apparent that Alzheimer's disease increases with age. It is by no means a rare disease affecting younger patients, as Alois Alzheimer himself had believed. Fears arose that demographic change – more and more older people and fewer and fewer young people – could lead to an explosion in patient numbers. This prompted the US to establish the National Institute on Aging (NIA) in 1974. In 1976, Robert Katzman († 2008), a pioneer in Alzheimer's research, identified Alzheimer's disease as the most common form of dementia, accounting for 60 percent of all cases. In 1980, the world's first Alzheimer's society, the Alzheimer's Association, was founded in the USA. Four years later, funding began for a network of Alzheimer's centers.
In 1984, George Glenner († 1995) and Caine Wong from the University of California in San Diego published findings showing that a peptide called Beta-amyloid is the main component of the Plaques – the first prime suspect for triggering nerve cell damage. Three years later, Konrad Beyreuther, Benno Müller-Hill († 2018) and their colleagues at the University of Cologne showed that the beta-amyloid peptide is formed by cleavage from a large precursor protein, the amyloid precursor protein (APP).
The role that APP plays in a healthy body is still not fully understood. One of its best-documented functions is its involvement in the formation, maintenance, and repair of synapses, the contact points between nerve cells. It also appears to protect neurons from harmful influences.
If APP is cleaved enzymatically in a certain way, beta-amyloid peptide may be released. This can clump together to form plaques. It is believed that an intermediate product in the formation of the plaques, known as oligomers, damages neighboring nerve cells and, above all, synapses. The “beta-amyloid hypothesis” has gained more and more supporters over the years. They are called “Baptists” in the research community.
In 1986, Inge Grundke-Iqbal († 2012) and colleagues from the New York State Office for People with Developmental Disabilities (OPWDD) published a very interesting paper. According to their findings, a protein called “tau,” which is associated with certain cytoskeletal proteins called microtubules, is a component of neurofibrils, the thread-like structures within cells. Tau appears to be the second main suspect. The “tau hypothesis” is supported by the “tauists.” According to Eckhard and Eva-Maria Mandelkow from the German Center for Neurodegenerative Diseases in Bonn, tau plays an important role in healthy bodies: “It stabilizes the microtubules, which are particularly important for transport processes in nerve cells. In Alzheimer's disease, tau falls off the microtubules, clumps together to form neurofibrils, and the Microtubules become unstable.”
Alzheimer's disease
Morbus Alzheimer
Alzheimer's disease is a progressive neurodegenerative disorder characterized by cortical atrophy, nerve cell loss, synapse loss, and deposits of amyloid plaques and neurofibrillary tangles, leading to dementia and loss of function. Early symptoms include memory problems, speech disorders, executive deficits, depressive moods, and subtle personality changes. As the disease progresses, global cognitive impairment, aphasia, agnosia, apraxia, and behavioral abnormalities such as apathy, restlessness, and sleep disorders occur. The disease was first described in 1907 by Alois Alzheimer.
Beta-amyloid
A peptide consisting of 36 to 42 amino acids that is considered the main component of senile plaques and is believed to be responsible for the development of Alzheimer's disease. The starting product is the amyloid precursor protein (APP). Certain enzymes in the cell membrane cut the precursor protein into peptides of various sizes. Amyloids consisting of 40 and 42 amino acids are found in senile plaques, with the 42-amino-acid product forming aggregates particularly quickly, at least in the Petri dish. The normal function of beta-amyloid has not yet been conclusively clarified.
Plaques
Senile plaques
Senile plaques accumulate in the gray matter of the brain when a protein – known as amyloid precursor protein – is not broken down correctly. Inflammation and disorders of fat or sugar metabolism can promote plaque formation. On average, the deposits reach a diameter of 50 micrometers. The appearance of plaques is one of several anatomical changes in the brain that pathologists can use to diagnose Alzheimer's disease after death.
Microtubules
Microtubules are one of the main components of the cytoskeleton, which gives cells stability and support. They consist of many copies of the proteins alpha- and beta-tubulin, which pair up to form tubes with a diameter of 20 to 30 nanometers. In addition to their supporting function, microtubules play an important role in transporting messenger substances through the cell. In neurons, for example, vesicles filled with neurotransmitters move along them to the synapses. In the nerve cells of the brains of Alzheimer's patients, a protein called tau can no longer stabilize the microtubules properly. As a result, they disintegrate, which contributes significantly to the development of dementia.
Beta-amyloid
A peptide consisting of 36 to 42 amino acids that is considered the main component of senile plaques and is believed to be responsible for the development of Alzheimer's disease. The starting product is the amyloid precursor protein (APP). Certain enzymes in the cell membrane cut the precursor protein into peptides of various sizes. Amyloids consisting of 40 and 42 amino acids are found in senile plaques, with the 42-amino-acid product forming aggregates particularly quickly, at least in the Petri dish. The normal function of beta-amyloid has not yet been conclusively clarified.
Alzheimer's disease
Morbus Alzheimer
Alzheimer's disease is a progressive neurodegenerative disorder characterized by cortical atrophy, nerve cell loss, synapse loss, and deposits of amyloid plaques and neurofibrillary tangles, leading to dementia and loss of function. Early symptoms include memory problems, speech disorders, executive deficits, depressive moods, and subtle personality changes. As the disease progresses, global cognitive impairment, aphasia, agnosia, apraxia, and behavioral abnormalities such as apathy, restlessness, and sleep disorders occur. The disease was first described in 1907 by Alois Alzheimer.
Other causes come into play
The joint occurrence of Plaques and Neurofibrils is characteristic of Alzheimer's disease The debate over which of the two events is the cause has shaped research for years. The current consensus is that the plaques form first, but that the cognitive deficits in Alzheimer's are closely related to the amount and distribution of tau fibrils.
It is still unclear what causes these initially harmless proteins to become pathological. We all produce amyloid from the very beginning, even as babies in the womb. Production alone does not lead to Alzheimer's pathology – it is a normal process. However, the chance of Beta-amyloid clumping together and forming plaques probably increases with age.
But according to Eckhard Mandelkow, Alzheimer's dementia is “not a disease based solely on tau or beta-amyloid.” There are many other possible reasons that “have something to do with it.” “Alzheimer's dementia is a multifactorial disease. Population studies have shown that there are several factors that increase the risk of Alzheimer's disease. Examples include high blood pressure and obesity.” These lead to vascular damage and, as a result, reduced blood flow to the brain. This impairs the energy supply to the nerve cells. Mandelkow: “That's why recommending a healthy lifestyle is actually the best thing you can do.”
Inflammatory processes are also involved in the development of Alzheimer's, as are disorders of the mitochondria, the “power plants” of the cells. In addition to these factors, genetic risk factors and certain epigenetic influences have also been identified. However, changes in individual genes that lead to the so-called familial form of Alzheimer's dementia are responsible for less than one percent of patients.
One thing is certain today. Eckhard Mandelkow puts it this way: “Aging is the most important risk factor. But the risk can be reduced: what is good for the heart is also good for the brain.”
Plaques
Senile plaques
Senile plaques accumulate in the gray matter of the brain when a protein – known as amyloid precursor protein – is not broken down correctly. Inflammation and disorders of fat or sugar metabolism can promote plaque formation. On average, the deposits reach a diameter of 50 micrometers. The appearance of plaques is one of several anatomical changes in the brain that pathologists can use to diagnose Alzheimer's disease after death.
Neurofibrils
Neurofibrils are fine fibrous structures in nerve cells that consist mainly of neurofilaments (a form of intermediate filaments) and other components of the cytoskeleton. They run in bundles through the cell body and the extensions of neurons and contribute significantly to the stabilization and shaping of the nerve cell. They appear as characteristic features of neurons even in the early embryo.
Alzheimer's disease causes profound changes in cytoskeletal structures: the protein tau, which normally stabilizes microtubules, becomes excessively phosphorylated, detaches from the microtubules, and aggregates to form the typical neurofibrillary tangles (fibrillary bundles). These are a central pathological feature of the disease.
Alzheimer's disease
Morbus Alzheimer
Alzheimer's disease is a progressive neurodegenerative disorder characterized by cortical atrophy, nerve cell loss, synapse loss, and deposits of amyloid plaques and neurofibrillary tangles, leading to dementia and loss of function. Early symptoms include memory problems, speech disorders, executive deficits, depressive moods, and subtle personality changes. As the disease progresses, global cognitive impairment, aphasia, agnosia, apraxia, and behavioral abnormalities such as apathy, restlessness, and sleep disorders occur. The disease was first described in 1907 by Alois Alzheimer.
Beta-amyloid
A peptide consisting of 36 to 42 amino acids that is considered the main component of senile plaques and is believed to be responsible for the development of Alzheimer's disease. The starting product is the amyloid precursor protein (APP). Certain enzymes in the cell membrane cut the precursor protein into peptides of various sizes. Amyloids consisting of 40 and 42 amino acids are found in senile plaques, with the 42-amino-acid product forming aggregates particularly quickly, at least in the Petri dish. The normal function of beta-amyloid has not yet been conclusively clarified.
dementia
Dementia
Dementia is an acquired deficit of cognitive, social, motor, and emotional abilities. The most well-known form is Alzheimer's disease. "De mentia" means "without mind" in English.
vascular
The term refers to vessels in the body in which fluids such as blood or lymph circulate. In a narrower sense, doctors refer to the network of veins, arteries, and capillaries as the "vascular system." If the vascular system is blocked, for example as a result of a stroke, less blood reaches the brain. This means that it receives less oxygen and other nutrients. This can lead to impaired cognitive functions and the development of "vascular dementia." After degenerative forms of dementia such as Alzheimer's, vascular dementia is the second most common form of this group of diseases.
Research gains momentum in the 1990s
In 1987, hope for improvement arises. The first test of a drug for Alzheimer's symptoms begins in the USA: Tacrin is based on the modulation of a Neurotransmitter (Acetylcholine) and its receptors. It compensates for the lack of acetylcholine that occurs in Alzheimer's disease due to the death of cholinergic neurons. However, its effectiveness is low, and tacrine, which was approved in 1993, has since been withdrawn from the market in many countries due to its side effects. Also in 1993, Allen Roses († 2016) and colleagues at Duke University in North Carolina published an important paper: they demonstrated that APOE-e4, a form of the apolipoprotein E Gene on chromosome 19, increases the risk of developing Alzheimer's dementia.
The following year, the disease took on a new face when Ronald Reagan announced his diagnosis to the public.
As early as 1980, associations were formed in Canada and the US to support Alzheimer's research and patients. In Germany, the first private association, the Alzheimer Forschung Initiative e.V., was founded in 1995, followed in 2000 by the Hans und Ilse Breuer-Stiftung. Finally, in 2009, Alzheimer's Disease International (ADI), the umbrella organization for Alzheimer's societies worldwide, published the first World Alzheimer Report. It paints a bleak picture.
Neurotransmitter
A neurotransmitter is a chemical messenger, an intermediary substance. It is released by the sender neuron at the sites of cell-cell communication and has an excitatory or inhibitory effect on the receiver neuron.
Acetylcholine
Acetylcholine is one of the most important neurotransmitters in the nervous system. In the central nervous system, it is involved in attention, learning, and memory; in the peripheral nervous system, it transmits excitation from nerves to muscles at the neuromuscular end plates and controls processes of the autonomic nervous system, i.e., the sympathetic and parasympathetic parts. Areas in which acetylcholine acts as a messenger substance are called cholinergic. It was the first neurotransmitter to be discovered, identified in 1921 by Otto Loewi in the heart of a frog.
Alzheimer's disease
Morbus Alzheimer
Alzheimer's disease is a progressive neurodegenerative disorder characterized by cortical atrophy, nerve cell loss, synapse loss, and deposits of amyloid plaques and neurofibrillary tangles, leading to dementia and loss of function. Early symptoms include memory problems, speech disorders, executive deficits, depressive moods, and subtle personality changes. As the disease progresses, global cognitive impairment, aphasia, agnosia, apraxia, and behavioral abnormalities such as apathy, restlessness, and sleep disorders occur. The disease was first described in 1907 by Alois Alzheimer.
cholinergic
Cholinergic neurons produce acetylcholine (an important neurotransmitter in the brain), and cholinergic synapses use it to transmit signals.
Gene
Information unit on DNA. Specialized enzymes translate the core component of a gene into ribonucleic acid (RNA). While some ribonucleic acids perform important functions in the cell themselves, others specify the order in which the cell should assemble individual amino acids into a specific protein. The gene thus provides the code for this protein. In addition, a gene also includes regulatory elements on the DNA that ensure that the gene is read exactly when the cell or organism actually needs its product.
dementia
Dementia
Dementia is an acquired deficit of cognitive, social, motor, and emotional abilities. The most well-known form is Alzheimer's disease. "De mentia" means "without mind" in English.
Dementia: increasing social and economic relevance
While the number of dementia patients was estimated at 35.6 million in 2010, it had already risen to 57 million by 2019, and the latest projections indicate that it is expected to increase to 152.8 million by 2050. The increase is not only due to demographic change, but also to increased awareness: this increases the likelihood of an Alzheimer's diagnosis, as it creates the conditions for access to treatment and care.
With better detection and care for patients, costs are also rising: in 2019, the cost of all types of dementia was estimated at approximately $1.3 trillion. And so, after 106 years, Alzheimer's disease has gone from being a marginal phenomenon to a problem that has reached the center of society. Society is now beginning to grapple with the implications.
dementia
Dementia
Dementia is an acquired deficit of cognitive, social, motor, and emotional abilities. The most well-known form is Alzheimer's disease. "De mentia" means "without mind" in English.
Alzheimer's disease
Morbus Alzheimer
Alzheimer's disease is a progressive neurodegenerative disorder characterized by cortical atrophy, nerve cell loss, synapse loss, and deposits of amyloid plaques and neurofibrillary tangles, leading to dementia and loss of function. Early symptoms include memory problems, speech disorders, executive deficits, depressive moods, and subtle personality changes. As the disease progresses, global cognitive impairment, aphasia, agnosia, apraxia, and behavioral abnormalities such as apathy, restlessness, and sleep disorders occur. The disease was first described in 1907 by Alois Alzheimer.
The therapy of the future: as multifactorial as the disease itself
Diagnostic capabilities have improved enormously over the years. Imaging techniques such as Magnetic resonance imaging make even the smallest changes in the brain visible. And with a special variant of positron emission tomography, radiologists can even visualize deposited amyloid and quantify its amount.
Biomarkers in the Cerebrospinal fluid (CSF) also provide clues about the disease process. Particularly informative is the ratio of two amyloid components, the Aβ42/Aβ40 ratio, as well as the concentration of tau and its phosphorylated variant (p-tau). While these samples still have to be obtained by lumbar puncture, in which fluid is extracted from the lumbar spine using a thin needle, a simpler procedure could soon become established: a blood test already approved in the USA also measures p-Tau and the Aβ42/Aβ40 ratio.
However, the greatest progress in recent years has been made with antibodies that target amyloid and can slow the progression of the disease. Donanemab and lecanemab are the first causal therapies to become available – with the caveat that these drugs are likely to benefit only a small proportion of patients for the time being. The reason for this, in addition to the high price of around €20,000 per year, is the numerous advanced imaging examinations that are necessary to detect any side effects at an early stage.
Therefore, referring to the possibilities of prevention remains the best advice at present. According to Hans Förstl, former director of the Clinic and Polyclinic for Psychiatry and Psychotherapy at the Klinikum rechts der Isar, good prevention includes the following: “It is very important to stimulate the brain. Not with mindless brain training, but with everything that brings people joy.” What is often neglected, he says, is the treatment of comorbidities that additionally impair mental performance.
Much has improved in the meantime. While the first drugs could only slightly delay the progression of the disease, their successors act directly against the amyloid deposits. They can significantly reduce existing deposits and slow down the formation of new ones. Over a period of 18 months, mental decline and the loss of everyday functions are slowed down by a quarter to a third. And there is hope that starting therapy even earlier will significantly delay the onset of severe symptoms.
Magnetic resonance imaging
Magnetic resonance imaging scanner
A device used by medical professionals for magnetic resonance imaging (MRI). MRI is an imaging technique used to diagnose malformations in various tissues or organs of the body. This method is particularly effective for imaging parts of the body that contain a lot of water. Patients are placed in a tube (scanner) and exposed to a strong magnetic field. However, they are not exposed to X-rays or other forms of ionizing radiation.
Cerebrospinal fluid
liquor cerebrospinalis
A clear fluid that fills the ventricular system and bathes the brain and spinal cord in the subarachnoid space, protecting them from impact. Three to five times a day, 100 to 160 ml of fluid is renewed by the choroid plexus. Certain diseases are reflected in the composition of the cerebrospinal fluid.
Further reading
- Alzheimer’s[MS2] Association (USA): Very comprehensive and layman-friendly texts, infographics, videos, interactive tools. Good mix of basic knowledge, diagnostics, therapy, care, prevention. Many printable PDF fact sheets; to the website.
- Alzheimer’s Disease International (ADI): Publisher of the World Alzheimer Reports; to the website.
- Mayo Clinic – Alzheimer’s Disease Center: Clear, medically reviewed articles. Well structured according to symptoms, diagnosis, and treatment. Very clear symptom and progression tables; to the website.
First published on September 18, 2013
Last updated on October 20, 2025
