The Basics Of Alzheimers Disease
Scientists are conducting studies to learn more about plaques, tangles, and other biological features of Alzheimers disease. Advances in brain imaging techniques allow researchers to see the development and spread of abnormal amyloid and tau proteins in the living brain, as well as changes in brain structure and function. Scientists are also exploring the very earliest steps in the disease process by studying changes in the brain and body fluids that can be detected years before Alzheimers symptoms appear. Findings from these studies will help in understanding the causes of Alzheimers and make diagnosis easier.
One of the great mysteries of Alzheimers disease is why it largely affects older adults. Research on normal brain aging is exploring this question. For example, scientists are learning how age-related changes in the brain may harm neurons and affect other types of brain cells to contribute to Alzheimers damage. These age-related changes include atrophy of certain parts of the brain, inflammation, blood vessel damage, production of unstable molecules called free radicals, and mitochondrial dysfunction .
When Was Alzheimers Disease First Discovered
Alois Alzheimer was a German psychiatrist and clinical researcher who at the turn of the last century studied a 50-year-old woman, known as Auguste D. , who exhibited signs of paranoia, confusion, crying fits, memory disturbance, and aggression upon her admittance to the Frankfurt Psychiatric Hospital where he worked.
Alzheimer documented her stay in the hospital and the progression of her symptoms. When she died five years later, Alzheimer conducted a histology of her brain tissue and found distinctive plaques.
The disease, whichthen carried Alzheimers name, was referred to as presenile dementia with some unusual histological signs and was considered very rare at the time. A few years later, Dr. Alzheimer studied the brain tissue of a male patient who had plaques similar to Auguste D.
A century after Dr. Alzheimer first discovered these neurological plaques, researchers continue to study the causes and effects of the terrible disease which bears his name with great hope for prevention and a cure.
Researchers Have Identified A New Type Of Dementia
In May, an international team of researchers identified a brain disorder known as LATE. It has similar symptoms to Alzheimers disease but appears to be caused by the build up of the toxic protein TDP-43.
Our researchers were able to delve into this particular protein by studying human brain tissue through our initiative Brains for Dementia Research.
The finding will help us distinguish between different brain disorders and develop precise and personalised treatments.
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A New Theory For Alzheimer’s
Some researchers are pinning hopes on another protein called tau.
If amyloid beta is the trigger, tau may be the bullet.
“Tau is one of my favourite proteins, where there’s tau there’s cell death in the brain,” says Prof Spires-Jones.
“I think tau is very important for somehow causing the cells to get sick and die.”
However, again this is not 100% certain and there is no evidence in human trials that lowering levels of tau in the brain is going to stop neurones dying.
Focusing on neurones and dangerous proteins can miss the bigger picture of what is happening in the brain.
This is a lesson being learned from cancer, where understanding the role the immune system plays has led to a whole new branch of medicine – cancer immunotherapy.
The immune system is being heavily implicated in dementia too.
If you look at genetic mutations that increase the risk of developing dementia, then a good chunk of them are involved in the immune system.
While your brain is packed with neurones that do the “thinking” – they are ably assisted by special immune cells called microglia.
They do fight infections, but also keep the brain running smoothly by munching up anything that should not be there.
And the blood vessels in the brain are increasingly being seen as a key player, not just in vascular dementia, but other dementias too.
“That’s what at this moment is happening.”
From Frankfurt To Munich Via Heidelberg
Apart from his very intensive clinical work, Alzheimer – together with Sioli – organized the establishment of a special branch hospital for mental patients close to Frankfurt in the Taunus mountains. In addition, he began to write a so-called Habilitationssdirift as a basis for an application at a medical faculty of a German university. He was in possession of the clinical and the postmortem findings of 320 patients with the diagnosis of Progressive Paralyse , investigated at the Frankfurt Hospital since 1888.
In the summer of 1902, little more than one year after the death of Alzheimer’s wife, Emil Kraepelin invited him to join the Heidelberg research team as assistant to the Heidelberg Hospital. This was a great honor because Kraepelin was at the time one of the most, prominent and influential psychiatrists in Germany. In addition, Alzheimer’s great friend Nissl had then been working in the Heidelberg Hospital for 7 years. In spite of many reasons in favor of Heidelberg, Alzheimer refused Kraepelin’s invitation and applied – unsuccessfully – for the leading position in a Hessian state hospital.
When Nissl heard about, this, he persuaded Kraepelin to repeat his offer of a position at the Heidelberg Hospital to Alzheimer. Kraepelin did so and Alzheimer accepted he moved to Heidelberg at the end of 1902.
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Rank Of Death Caused By Alzheimers Disease
Rank of death caused by Alzheimers disease found to be a lot more than reported on death certifications. Scientists at Rush College locate that the annual number of deaths due to Alzheimers disease in the UNITED STATE among individuals a minimum of 75 years of ages is about 500,000, a lot greater than the number reported on death certificates .
Framing Dementia As A Brain Disease In Early Twentieth
In the mid-nineteenth century, psychiatry in Europe and America was seen by many as falling behind other branches of clinical medicine that were rapidly progressing in their ability to define the pathogenesis and etiology of discrete disease entities through pathological and eventually bacteriological research . The discovery by German psychiatrists in 1857 that general paresis, one of the most common forms of what was then called insanity, was connected to syphilitic infection raised new hopes that clinical-pathological correlations would lead to etiological theories and ultimately therapeutic interventions for other forms of mental illness .
In the first decade of the twentieth century, the German psychiatrists Emil Kraepelin and Alois Alzheimer were interested in making dementia the second major mental disorder for which a clear pathological basis had been established. In 1906, Alzheimer presented a brief paper on the case of a 51-year-old woman who developed progressive dementia that, despite her young age, seemed to be identical to senile dementia. In 1910, on the basis of this case and a handful more published by Alzheimer and others, Alzheimers mentor Emil Kraepelin created the category of Alzheimers disease in the eighth edition of his influential textbook to distinguish early-onset presenile cases occurring before age 65 from the much more common senile dementia occurring at later ages .
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How Is Alzheimer’s Disease Diagnosed
There is currently no single test to identify Alzheimer’s disease. The diagnosis is made only after careful clinical consultation.
The clinical diagnosis might include:
- A detailed medical history
- Lumbar puncture for cerebral spinal fluid tests
- Medical imaging
These tests will help to eliminate other conditions with similar symptoms such as nutritional deficiencies or depression. After eliminating other causes, a clinical diagnosis of Alzheimer’s disease can be made with about 80% to 90% accuracy if the symptoms and signs are appropriate. The diagnosis can only be confirmed after death by examination of the brain tissue.
It is important to have an early and accurate diagnosis to determine whether a treatable condition other than Alzheimer’s disease, is causing the symptoms. If Alzheimer’s disease is diagnosed, medical treatment and other assistance can be discussed.
The Story Of Auguste Deter
I have lost myself, so to say.
Such was the response Auguste Deter would continually give when asked questions she could no longer answer.
Dr. Alzheimer became fascinated with Deters condition, initially diagnosing her with presenile dementia. Alzheimer asked Auguste questions that were similar to those that would be asked by a doctor today who was screening for the disease named for him. When asked what her name was, she would respond Auguste, but then when asked what her husbands name was, she would give her own name again. While she had the ability to recognize and name some objects, like a pencil, a key, a cigar, when asked what she was eating she would reply spinach even though she was eating pork.
During her 5-year stay at the institution, her condition worsened to the point where she lost almost all cognitive ability. On April 8, 1906, at age 55, Auguste passed away.
If Auguste had been alive today, she would have been diagnosed with early-onset Alzheimers disease. This form of Alzheimers is rare and accounts for less than 10% of all cases of the disease. Alzheimers disease is usually not recognized until around age 65.
At American Senior Communities, we have created a special memory care program called , which focuses on the social model philosophy of care. We focus on maintaining a home-like environment that is secure, yet gives residents a sense of belonging. Augustes Cottages are located throughout the state.
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If I Live Long Enough Will I Get Dementia
Not necessarily.
There used to be a public perception that dementia was a normal part of the ageing process.
However, the research is clear – dementia is caused by disease.
And some people who live well into their 90s and beyond have brains that remain remarkably clear of any signs of dementia.
Prof Tara Spires-Jones, the deputy director of the centre for discovery brain sciences at the University of Edinburgh, said: “I think there are some people who would be fine, even if they lived for another 100 years.”
Invention Of The Electron Microscope Permits Further Study Of The Brain
In 1931, the two Germans Max Knoll and Ernst Ruska made the electron microscope, which can multiply up to 1 million times. It is not up until after WWII that the electron microscopic becomes common in major research study setups, allowing scientists to study brain cells in more detail.
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How Early Onset Dementia Led To A Historic Discovery
When Alois Alzheimer described the case of Auguste D. to an audience of fellow psychiatrists in Tuebingen, Germany, in 1906, what set her case apart was the fact that her dementia appeared before she was 50 years old. Dementia at a more advanced age was considered part of normal aging. But this relatively young German hausfrau’s increasingly disruptive behavior caused her distraught husband to bring her in for a doctor’s examination when she was 51. It fell upon Dr. Alzheimer to follow her case. Alzheimer’s mentor Emil Kraepelin of Munich, the foremost psychiatrist in his day, promoted the fundamental insight that dementia is a physical, organic disease of the brain, so when Auguste D. died, Alzheimer examined her brain for unusual pathology. At the time, based on the contemporary theories of Freud, psychotic or “crazy” behavior was thought to result from psychodynamic causes, so Alzheimer’s discovery of plaques and tangles in Auguste D.’s brain was a landmark . The German medical literature of the time recognized that this mid-life dementia was more common in certain families, so the idea of familial Alzheimer disease goes back to those days, as well.
Making Breakthroughs Possible Today
While these are some notable examples of progress, dedicated dementia researchers are making advances every day and your support is making their work possible.
With your continued support, our mission is bold and clear to continue to power incredible discoveries in research and translate them into breakthroughs that change the lives of people with dementia. Find out more.
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Medications For Vascular Dementia
Because vascular dementia is caused by the death of brain tissue and atherosclerosis, there is no standard drug treatment for it. Drugs used to treat other atherosclerotic vascular diseases such as cholesterol medications, blood pressure medications, and anti-blood clotting medications, may be used to slow the progression of vascular dementia. In some cases, cholinesterase inhibitors and antidepressants may help improve symptoms associated with vascular dementia.
Why Is It Becoming More Common
The answer is simple – we are living longer and the biggest risk factor for dementia is age.
That is why huge increases in dementia cases are predicted for Asia and Africa.
With a more philosophical hat on, you can see dementia as the price we pay for progress in treating deadly infections, heart attacks and cancer.
Although there is an unexpected and hopeful trend emerging that has surprised some in the field – the proportion of elderly people getting dementia is falling in some countries.
Studies have shown the dementia rate falling in the UK, Spain and the US and stabilising in other countries.
This is largely being put down to improvements in areas like heart health and education which in turn benefit the brain.
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Alzheimer’s Disease: The Progress Of Naming
Alzheimer’s Disease is named after the widely known doctor who focused on the study of neurosyphilis and vascular dementia. He reported the first case to the academic world. As Alzheimer’s disease is common in contemporary medicine, the origin and progress of naming, Alzheimer’s Disease, are described in detail.,,,,,,,
Is There Anything I Can Do To Dodge Dementia
There are no guarantees, but there are ways you can lower the odds of developing dementia.
- don’t develop type 2 diabetes
It is not completely clear why these protect the brain.
Do these lifestyle factors actually stop the process of dementia in the brain?
Or do they prepare the brain for dementia by increasing the connections and flexibility of the brain so that as neurones start to die, the brain can compensate for longer and symptoms don’t emerge?
On a personal level it probably doesn’t matter – not getting dementia, is not getting dementia. But scientifically the questions matter as the answers will illuminate what is going on in the brain.
“People who are very healthy and take good care of themselves are the group that I would say is most resilient to Alzheimer’s disease,” says Prof Spires-Jones.
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Why Is There Such A Gap In Our Knowledge
There are two significant factors – one is the sheer complexity of the brain and the other is a lack of funding for research.
The human brain is the most complex structure in the known universe and is made up of 100 billion neurones.
To steal Prof de Strooper’s analogy if every person on the planet had a computer and they were all hooked up and working together – that would still be less than a tenth of what’s going on inside the brain.
And yet for every single scientific study published on any form of neurodegeneration, there are 12 on cancer.
The focus has simply been elsewhere.
The First Use Of Alzheimers Disease
Alzheimer later published his descriptions of several similar patients in 1909 and Kraepelin included Ms. Deters case in the 1910 edition of his widely respected psychiatry textbook. It was Kraepelin who named this dementia after his junior colleague.Auguste Deter was not an elderly woman at the onset of her illness, and Alzheimers disease was therefore regarded as a presenile dementia to distinguish it from the familiar senile dementia thought to result from aging-related vascular disease. Further investigation, however, showed that plaques and tangles were present in the brains of the majority of older adults with symptoms of dementia.
In the late 1960s, the British psychiatrists Tomlinson and Roth described the importance of these plaques in older adults, and in 1970 Dr. Roth questioned the meaningfulness of the age criterion that distinguished AD from senile dementia of the Alzheimers type.
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How Is Alzheimers Disease Treated
Alzheimers is complex, and it is therefore unlikely that any one drug or other intervention will successfully treat it in all people living with the disease.
Scientists are exploring many avenues to delay or prevent the disease as well as to treat its symptoms. In ongoing clinical trials, scientists are developing and testing several possible interventions. Under study are drug therapies aimed at a variety of disease interventions, as well as nondrug approaches such as physical activity, diet, cognitive training, and combinations of these. Just as we have many treatments for heart disease and cancer, we will likely need many options for treating Alzheimers. Precision medicine getting the right treatment to the right person at the right time will likely play a major role.
Current approaches to treating Alzheimers focus on helping people maintain mental function, treating the underlying disease process, and managing behavioral symptoms.
Framing Dementia As A Dread Disease And Major Public Health Crisis In An Aging World
Dementia emerged as a major public issue in the late 1970s through the efforts of a coalition of caregivers and family members struggling to deal with dementia in the context of new expectations for aging, researchers in the neurosciences influenced by the biological revolution in psychiatry, and government officials trying to win funding for research on aging and age-associated conditions. Central to the coalitions strategy was advancing the claim that age-associated dementia should be viewed as the result of disease rather than aging, as part of a more general claim advanced within gerontology and geriatrics that aging itself should not normally be accompanied by disease and disability . Neurologist Robert Katzman was perhaps the most prominent exponent of this claim, arguing in an influential 1976 article that the distinction between what was then called Alzheimers presenile dementia and senile dementia ought to be dropped and that the unified entity should be called Alzheimers disease .
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