After 57 years of marriage, an old man “exhausted” from caring for his Alzheimer’s sick wife shoots her to death

The authorities brought murder charges to a 80 year old man in Nebraska who told the police that he shot and killed his wife, who had Alzheimer, because he was having trouble taking care of her.

Prosecutors raised charges against John Kotopka Wednesday to premeditated murder a week after the death of 78-year-old Janet Kopotka. He had originally been charged with assault for shooting her at his home in Lincoln on June 20.

Janet Kotopka He received a diagnosis of Alzheimer’s disease two years ago and his health had deteriorated considerably, according to court documents. John Kotopka told investigators that he was “exhausted and could no longer care for her” and that he feared the potential financial burden of sending her to a nursing home.

He also said that he began to think about killing his 57-year-old wife about 10 days before doing so.

Kotopka is being held in the Lancaster County Jail without bond and has not yet pleaded guilty or not guilty. His attorney, John Berry, said the incident is a horrible tragedy for the family, but declined to comment on the details of the case.

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Protein accumulations in the reproductive system crucial? – healing practice

Sexual cell protein balance affects harmful protein deposition

Protein deposits in the body are associated with neurodegenerative diseases such as Alzheimer’s disease, Huntington’s disease or ALS (amyotrophic lateral sclerosis). In a recent study it has now become clear that the protein balance in the sex cells is apparently related to the protein accumulations elsewhere in the body.

Researchers at the University of Cologne and the University of California have jointly investigated to what extent the status of the protein balance (protein homeostasis or proteostasis) of germ cells influences other tissues and organs. This showed a clear effect on the formation of protein deposits, which also occur in some neurodegenerative diseases. The corresponding study results were published in the journal “Science Advances”.

Investigated protein homeostasis in roundworms

The research team around Dr. David Vilchez from the University of Cologne used the nematode Caenorhabditis elegans as a model organism to analyze how the protein homeostasis of germ cells influences other tissues and organs. To do this, they induced “the aggregation of the germline-specific PGL-1 protein in germline stem cells” of the nematode.

Protein deposition in muscles and neurons

It became clear that an accumulation of the protein in the germ cell leads to the release of certain signal messenger substances, which cause changes in the mitochondria via the Wnt signaling pathway. This regulation of the mitochondria can in turn lead to protein accumulation in other tissues such as muscles or neurons, the researchers report.

The mitochondrial network has changed dramatically

“We were very astonished to see that we can change the mitochondrial network of the entire organism simply by inducing protein clumps in germ cells. This change has also caused protein accumulations in neurons, ”emphasizes the first author of the study, Guiseppe Calculli from the University of Cologne.

“Our results open a new door to understanding why protein aggregates accumulate in the neurons of patients with Huntington’s disease and ALS,” added Dr. Vilchez. Since these aggregates can contribute to the neurodegeneration characteristic of these diseases, which is still incurable, “a further understanding of the process discovered here could lead to new therapeutic approaches.”

Basis for further studies

In the current study it became clear that the “proteostatic status of germline stem cells influences mitochondrial networks and protein aggregation in the entire organism”, summarize the researchers. Whether germ-specific proteins also accumulate during the aging process and whether this process contributes to the age-associated aggregation of proteins that is characteristic of diseases such as Huntington’s disease or ALS must now be investigated in further research. (fp)

Author and source information

This text complies with the requirements of specialist medical literature, medical guidelines and current studies and has been checked by medical professionals.

Swell:

  • University of Cologne: Protein balance in the reproductive system can prevent diseases (published June 25, 2021), uni-koeln.de
  • Giuseppe Calculli, Hyun Ju Lee, Koning Shen, Uyen Pham, Marija Herholz, Aleksandra Trifunovic, Andrew Dillin, David Vilchez: Systemic regulation of mitochondria by germline proteostasis prevents protein aggregation in the soma of C. elegans; in: Science Advances (veröffentlicht 25.06.2021), sciencemag.org

Important NOTE:
This article is for general guidance only and is not intended to be used for self-diagnosis or self-treatment. He can not substitute a visit at the doctor.

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Is protein status crucial in the reproductive system? – healing practice

Sexual cell protein balance affects harmful protein deposition

Protein deposits in the body are associated with neurodegenerative diseases such as Alzheimer’s disease, Huntington’s disease or ALS (amyotrophic lateral sclerosis). In a recent study it has now become clear that the protein balance in the sex cells is apparently related to the protein accumulations elsewhere in the body.

Researchers at the University of Cologne and the University of California have jointly investigated to what extent the status of the protein balance (protein homeostasis or proteostasis) of germ cells influences other tissues and organs. This showed a clear effect on the formation of protein deposits, which also occur in some neurodegenerative diseases. The corresponding study results were published in the journal “Science Advances”.

Investigated protein homeostasis in roundworms

The research team around Dr. David Vilchez from the University of Cologne used the nematode Caenorhabditis elegans as a model organism to analyze how the protein homeostasis of germ cells influences other tissues and organs. To do this, they induced “the aggregation of the germline-specific PGL-1 protein in germline stem cells” of the nematode.

Protein deposition in muscles and neurons

It became clear that an accumulation of the protein in the germ cell leads to the release of certain signal messenger substances, which cause changes in the mitochondria via the Wnt signaling pathway. This regulation of the mitochondria can in turn lead to protein accumulation in other tissues such as muscles or neurons, the researchers report.

The mitochondrial network has changed dramatically

“We were very astonished to see that we can change the mitochondrial network of the entire organism simply by inducing protein clumps in germ cells. This change also caused protein accumulations in neurons, ”emphasizes the first author of the study, Guiseppe Calculli from the University of Cologne.

“Our results open a new door to understanding why protein aggregates accumulate in the neurons of patients with Huntington’s disease and ALS,” added Dr. Vilchez. Since these aggregates can contribute to the neurodegeneration characteristic of these diseases, which is still incurable, “a further understanding of the process discovered here could lead to new therapeutic approaches.”

Basis for further studies

In the current study it became clear that the “proteostatic status of germline stem cells influences mitochondrial networks and protein aggregation in the entire organism”, summarize the researchers. Whether germ-specific proteins also accumulate during the aging process and whether this process contributes to the age-associated aggregation of proteins that is characteristic of diseases such as Huntington’s disease or ALS must now be investigated in further research. (fp)

Author and source information

This text complies with the requirements of specialist medical literature, medical guidelines and current studies and has been checked by medical professionals.

Swell:

  • University of Cologne: Protein balance in the reproductive system can prevent diseases (published June 25, 2021), uni-koeln.de
  • Giuseppe Calculli, Hyun Ju Lee, Koning Shen, Uyen Pham, Marija Herholz, Aleksandra Trifunovic, Andrew Dillin, David Vilchez: Systemic regulation of mitochondria by germline proteostasis prevents protein aggregation in the soma of C. elegans; in: Science Advances (veröffentlicht 25.06.2021), sciencemag.org

Important NOTE:
This article is for general guidance only and is not intended to be used for self-diagnosis or self-treatment. He can not substitute a visit at the doctor.

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Aducanumab is the first drug effective against Alzheimer’s disease?

Aducanumab is the new remedy, the first ever Alzheimer can slow down. It is approved in the USA – and highly controversial.


Alzheimer’s drug approved in the USA – will we soon?


For Alzheimer’s sufferers and their relatives it is the only glimmer of hope in a desperate situation, for the manufacturer Biogen a billion dollar business – for many scientists and doctors, aducanumab is one thing above all: too little researched.


Nevertheless, the American Food and Drug Safety Authority (FDA) approved the novel active ingredient against Alzheimer’s at the beginning of June 2021.

A medical sensation: The active ingredient aducanumab or Aduhelm (US brand name) is the first drug ever to fight the disease itself. In the case of Alzheimer’s dementia, only the symptoms, if at all, could be alleviated with medication. Now, in theory, aducanumab should slow down the progression of mental decline in every Alzheimer’s patient, regardless of the stage. A medicine revolution? It’s very controversial. This is not the only reason why it will take some time before the drug comes onto the market in Germany – if at all. Read here how the new Alzheimer’s drug works, everything about the research situation, and what makes aducanumab approval so problematic

How Alzheimer’s occurs and how aducanumab is supposed to stop it


Aducanumab is a monoclonal antibody, which means that it works in the body like a kind of vaccination. The goal of a normal vaccination is to produce antibodies that work against a pathogen. Alzheimer’s is not about viruses or bacteria that should be fought, but the goal is something else – the protein beta-amyloid. How Alzheimer’s occurs and why beta amyloid plays a major role in it:


To make the human brain so efficient, more than 100 billion nerve cells work together, constantly processing information and stimuli. So that the network works, the nerve cells are connected via contact points, so-called synapses. The exchange takes place via the synapses through messenger substances. You are the first to be affected by Alzheimer’s, so that the communication between the nerve cells no longer works properly – the first disturbances appear, e.g. increased forgetfulness, concentration and orientation problems.


This is how you can recognize the first signs of Alzheimer’s disease and act!


In the further course of the disease, nerve cells die completely, they are irretrievably lost. This leads to drastic symptoms, which can be very individual depending on the Alzheimer’s patient – also how quickly the disease progresses is very different. Alzheimer’s has four stages that can span up to 20 years. In the third and fourth stages, those affected often suffer from:


  • Loss of short-term memory and long-term memory disruption, e.g. sudden memories from childhood.
  • Loss of ability to recognize faces, including those of close relatives.
  • Disturbed sense of time and disturbed day / night rhythm.
  • Disorientation, nervousness, distrust, often the need to run away.
  • Talking, swallowing, and moving become difficult or impossible.

In short: the brain gradually stops functioning. But what destroys this once powerful organ? Despite intensive research, it is still not known exactly why some people develop Alzheimer’s and others do not. What is certain, however, is that two factors lead to the destruction of nerve cells: the protein beta-amyloid and the protein component tau protein.


Beta amyloid occurs naturally in the brain and is completely harmless in itself. Beta amyloid arises from a biochemical reaction. In Alzheimer’s disease, this process changes, so that defective beta-amyloid proteins are created. They accumulate and clump, thereby forming indissoluble deposits between the nerve cells, the plaques. In addition, there is a modified tau protein, i.e. a protein building block, in the nerve cells.


Tau proteins help move nutrients from one cell to another. In Alzheimer’s disease, the tau protein changes so that it is deposited in the nerve cell, causing it to lose its shape and break down.


Alzheimer’s goes back to the fact that nerve cells in the brain are damaged by protein deposits. This is where aducanumab comes in. The active ingredient reduces the plaques from the protein beta-amyloid in the brain, as studies clearly show. There is great disagreement about everything else.


Why the approval of the Alzheimer’s drug is so controversial


It was an unusual move by the US FDA – they have now granted aducanumab marketing authorization, but only on condition that further research takes place. Normally, all studies and tests with patients must be completed before a new drug can come onto the market. However, when it comes to treating Alzheimer’s, the situation is complex, not to say desperate. It is better to use a remedy that might just prevent patients from losing weight further than to have no remedy at all, so the argument of patient representatives and Alzheimer’s relatives. In addition, precious time should not be wasted. Because even aducanumab is not able to cure Alzheimer’s or reverse the damage, the disease can only be prevented from progressing – maybe.


How effective aducanumab really is is highly controversial and cannot yet be determined with certainty. Because it’s not clear whether a decrease in beta amyloid is really enough to stop Alzheimer’s disease. The clinical tests by the manufacturer Biogen do not show a clear picture, but rather two contradicting phase 3 studies. Phase 3 of approval studies is an examination with a large number of patients, one group of whom receives the new drug and another group is treated as usual or receives a placebo preparation. The comparison of the results should show whether the remedy is effective and also what side effects occur. In the case of aducanumab, a phase 3 study showed that the active ingredient could slightly slow down the mental decline in Alzheimer’s patients. Another study, however, showed no clear effect. As a result, the studies were stopped prematurely because aducanumab did not appear to have any benefits for those affected – it was unethical to continue exposing people to a novel drug with potential side effects if it does not help anyway.


However, manufacturer Biogen then stated that further data had been evaluated and found that a particularly high dose of aducanumab had positive effects after all. The decline in mental abilities and memory is said to have been slowed down by about 22 percent. This means that the mental decline, calculated over a period of one and a half years, could be postponed by about four months. After many debates from various scientific committees, the FDA has now decided to grant approval in order to give Alzheimer’s patients and their relatives the chance of more time in better health.


How do you rate the Alzheimer’s drug in Germany?


In this country people are a lot more cautious about the potential of aducanumab. The assessment of the Alzheimer Research Initiative eV, which promotes education and independent scientific research on Alzheimer’s:


“We welcome the decision of the FDA to approve the Alzheimer’s active ingredient aducanumab on the condition that the manufacturer Biogen submits another study on the effectiveness of the drug. (…) The approval shouldn’t raise false hopes. It does not cure the disease, it slows down the loss of memory to a small extent. For patients in a very early stage of the disease, this can temporarily noticeably stabilize their cognitive abilities and quality of life. “


So it doesn’t help, doesn’t it hurt? Unfortunately, no. Because even if Alzheimer’s patients are people at the end of their life, the possible side effects of aducanumab must not be forgotten. “The effect is offset by serious side effects and extensive and close-knit medical supervision. One side effect of the active ingredient is brain swelling, which can lead to cerebral hemorrhage undetected. Therefore, participants in the approval studies were examined at regular intervals with imaging procedures such as MRI the dose was suspended. Such accompanying examinations would also have to be carried out regularly on patients, “the Alzheimer Research Initiative points out.


Treatment would not be done with the administration of the drug, accompanying examinations could mean further stress, especially for Alzheimer’s patients, and make acceptance more difficult. Another problem is that although aducanumab can theoretically be used in any stage of Alzheimer’s disease, those affected often no longer have the mental abilities to actively choose it.


What will happen to the patient studies on aducanumab?


Aducanumab can currently only be prescribed in the USA, and there are no clinical studies on the active ingredient in this country that patients can participate in. The European Medicines Agency (EMA) will likely decide towards the end of the year whether aducanumab should be approved in the EU. The manufacturer Biogen had submitted an application for this.


The EMA first decides on approval on the basis of study data from the USA. There, Biogen was obliged to carry out additional studies after the market launch, which should clearly demonstrate how much aducanumab improves cognitive abilities. The company has nine years to do this. An approach that worries many scientists. They fear that it will be very difficult to find participants for a placebo-controlled study.


Why should Alzheimer’s patients get involved and maybe only get the dummy drug when they can simply get a prescription for aducanumab? Just one of the many stumbling blocks on the way to effective Alzheimer’s therapy. After all, two other active ingredients are currently in the trial phase and could come onto the market within the next few years, perhaps with greater effectiveness. The Alzheimer’s Research Initiative is cautiously optimistic about this new class of drugs:


“So far, there are no drugs in the drug therapy of Alzheimer’s disease that act on the basic mechanisms of the disease. The previous drugs stimulate brain performance, and side effects of the disease, such as depression, can be treated. Aduhelm takes action against this the protein deposits in the brain that are characteristic of Alzheimer’s disease. “


Anyway: Social contacts and exercise therapy help with depression in Alzheimer’s sufferers better than drugs, studies show.


Alzheimer’s is and will remain an incurable disease, which is one of the reasons why prevention is so important. After all, there is now some knowledge about measures that can protect you. This is especially important for women, because they are more often affected by Alzheimer’s disease.


You can find even more information on detection and prevention and also on the behavior of relatives on our Alzheimer’s topic page.


At the Alzheimer Research Initiative eV you will find explanations of the current state of Alzheimer’s research and medical background knowledge.



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Online calculator predicts the risk of dementia

Dr. Karen Zoufal | 06/25/2021

Canadian researchers have developed a dementia risk calculator that uses simple statements about health and lifestyle to estimate the likelihood of a dementia diagnosis within the next five years for people aged 55+. During the evaluation, the participants are also given tips on how to reduce the risk.

Dr. Stacey Fisher from the University of Toronto explained: “The special thing about this dementia risk calculator is that you don’t have to see a doctor. You already have all the information you need to fill out the computer conveniently at home. “

Data that have to be entered into the dementia risk calculator are e.g. B .:

  • Alter
  • Smoking status
  • Alcohol consumption
  • Physical activity
  • Stress
  • nutrition
  • Immigration status
  • Level of education
  • Activities where help is needed
  • marital status
  • Number of languages ​​spoken
  • Health information

“This tool gives people who fill it out pointers on what they can do to reduce their personal risk of dementia,” said Dr. Peter Tanuseputro of Ottawa Hospital.

The calculator is based on statistical data from the Canadian Health Authority and has been tested with survey data from over 75,000 people from Ontario. The calculator was developed for Canada, but can be adapted to the situation in other countries that collect health data.

Dementia is a collective term for various diseases that are associated with a loss of mental performance. A cure or treatment is not yet possible. However, around a third of cases could be avoided by following a healthy lifestyle with sufficient physical activity, a healthy diet, little alcohol, no smoking, and treatment for conditions such as diabetes and high blood pressure.

The online calculator in English is available at www.projectbiglife.ca/dementia.

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Too little sleep in middle age increases the risk of dementia – medical practice

Lack of sleep linked to risk of dementia

Health experts repeatedly emphasize how important restful sleep is for health and performance. For example, the brain should detoxify itself faster and rid itself of harmful substances during sleep. The results of a new long-term study now show that people who regularly sleep too little between the ages of 50 and 70 have an increased risk of developing dementia.

Researchers from University College London (UCL) and the French Institut national de la santé et de la recherche médicale (INSERM) come to the conclusion in a recent study that people who sleep six hours or less per night in their 50s and 60s , have a higher risk of developing dementia later in life. The study results were recently presented in the renowned journal “Nature Communications”.

Risk of dementia increased by 30 percent if there is a lack of sleep

According to the evaluation of the long-term study, in which 7,959 British adults were asked about their sleep times since 1985, those who between the ages of 50 and 70 years of age consistently slept six hours or less per night are about 30 percent higher risk of developing dementia to develop than those who slept longer. 521 of the participants had been diagnosed with dementia by the end of the study period in 2019.

Relationship between length of sleep and risk of dementia

“It is known that sleep problems occur in people with dementia, but it remains unclear whether the length of sleep in midlife influences the risk of developing dementia in old age,” reports lead author of the study, Dr. Séverine Sabia. The present study with a very long follow-up period shows that a short sleep duration in mid-life is associated with the risk of dementia later in life.

Underlying process not yet deciphered

“While we cannot confirm that too little sleep actually increases the risk of dementia, there are many reasons why a good night’s sleep could be good for brain health,” says Dr. Sabia. The results underscore the importance of proper sleep for health.

Why lack of sleep could trigger dementia

Even if the exact causes of the link between sleep duration and dementia risk are not adequately understood, there are some plausible indications. Sleep researchers have already shown, for example, that the spaces between the cells in the brain filled with brain water expand during deep sleep, which means that metabolic products that are no longer required can be transported out of the brain tissue at twice the speed.

In addition, beta-amyloid deposits were found more often in the brains of people with obstructive sleep apnea syndrome than in people who do not have sleep apnea. Such beta-amyloid plaques are linked to the development of Alzheimer’s disease.

Sleeping too much doesn’t seem to increase the risk of dementia

Previous studies also reported an increased risk of dementia in people who sleep longer than average. According to the researchers, however, the results were inconsistent. An increased risk of dementia with an above-average length of sleep could not be proven in the current study. “More studies, including more people who sleep long, are needed to understand the role length of sleep plays in the risk of dementia,” said the research team.

Sleep is important to health

“We know that sleep is important for the health of our brain, as it is involved in learning and memory, the removal of waste materials from the brain and the ability of our brain cells to stay healthy,” sums up lead author Dr. Archana Singh-Manoux. The findings could help to develop new ways of reducing the risk of dementia. (vb)

Author and source information

This text complies with the requirements of specialist medical literature, medical guidelines and current studies and has been checked by medical professionals.

Author:

Diploma-Editor (FH) Volker Blasek

Swell:

  • National Institute of Health and Medical Research: Dementia: shorter nights associated with an increased risk of developing the disease (veröffentlicht: 20.06.2021), presse.inserm.fr
  • University College London: Lack of sleep in middle age linked to dementia risk (veröffentlicht: 20.06.2021), ucl.ac.uk
  • Sabia, S., Fayosse, A., Dumurgier, J. et al. Association of sleep duration in middle and old age with incidence of dementia; in: Nature Commun. (2021)., nature.com
  • Deutsches Ärzteblatt: Middle-aged sleep deprivation announces a later risk of dementia (published: June 21, 2021), aerzteblatt.de

Important NOTE:
This article is for general guidance only and should not be used for self-diagnosis or self-treatment. He can not substitute a visit at the doctor.

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Alzheimer’s disease: iron nanoparticles in the brain – new findings

WFor the first time, scientists have detected nanocrystals made from pure iron and copper in the brains of deceased Alzheimer’s patients. It is still unclear what role these metals may play in the development of the disease. Researchers hope that Alzheimer’s can be diagnosed earlier in the future. In any case, the surprising research result opens up a new lead.

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Alzheimer’s Awareness Month.. 6 foods to improve brain health and increase focus

Every year in June, the world celebrates Alzheimer’s Disease Awareness Month, the most common type of dementia, where plaques form in the brain, which leads to a gradual loss of cognitive ability and a decline in the function of daily activities, and you can protect yourself from this disease and maintain brain health from While focusing on eating a healthy diet, in this report we learn about the most prominent foods that improve brain health and increase focus, according to the website ” today“.

Foods to improve brain health and increase focus

green leafy vegetables

Studies show that consuming green leafy vegetables, such as kale, watercress, spinach and collard greens, was linked to slower cognitive decline in older adults. One daily serving of green leafy vegetables was all it took to help slow brain aging.

grapes

Numerous animal and human studies have been conducted that support the beneficial effect of grapes on brain function. Grapes help promote healthy blood flow and blood pressure and reduce oxidative stress in the brain, all of which benefit brain health.

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Walnuts

As in other diseases, inflammation plays a major role in Alzheimer’s disease and other brain disorders.

Walnuts contain several compounds, including polyphenols, tocopherols and polyunsaturated fatty acids, that help fight inflammation and provide antioxidant benefits.

berries

One cup of berries provides vitamin C What the body needs daily, in addition to manganese and vitamin K and anthocyanins, which give baby berries their colorful skin, all for just 80 calories. Anthocyanins also play a role in protecting the brain.

Extra virgin olive oil

Olive oil contains phenols, a type of antioxidant that helps maintain brain health by reducing inflammation as well as protecting against Alzheimer’s disease. Studies have shown that olive oil offers benefit in other neurodegenerative diseases, including Parkinson’s disease and Alzheimer’s disease. Amyotrophic lateral sclerosis.

fatty fish

Fatty fish is one of the most well-documented foods for brain health. Fatty fish, including salmon, tuna, and herring, contain omega-3 fatty acids. gave A type of polyunsaturated fat, these acids protect the brain and help prevent the development of Alzheimer’s disease.

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Alzheimer’s disease: iron nanoparticles in the brain

WFor the first time, scientists have detected nanocrystals made from pure iron and copper in the brains of deceased Alzheimer’s patients. It is still unclear what role these metals may play in the development of the disease. Researchers hope that Alzheimer’s can be diagnosed earlier in the future. In any case, the surprising research result opens up a new lead.

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Alzheimer’s disease: iron nanoparticles in the brain

WScientists from Germany, Great Britain and the USA have discovered a new lead that could potentially lead to a better understanding of Alzheimer’s and how it develops. It has long been known that the disorder associated with memory disorders is associated with deposits of insoluble proteins in the brain. At least these so-called plaques, also known as amyloids, can be detected in the brains of deceased Alzheimer’s patients.

Scientists from TU Darmstadt, the University of Warwick, the University of Keele, the University of Texas in San Antonio and the Case Western Reserve University now report in the journal “Science Advances” that they have for the first time detected nanoparticles made of copper and iron in such plaques .

“The size of these particles is a few tens of nanometers,” explains Professor Frederik Lermyte from TU Darmstadt, “it was a great surprise for us to discover these metal particles in brain tissue. This is really new. “

also read

It has long been known, however, that water-soluble compounds of copper and iron play a role in brain metabolism. In their investigations, however, the researchers not only came across such molecules, but also insoluble nanoparticles made of pure metal.

The scientists used a number of measurement methods to prove this, including mass spectroscopy and X-ray absorption spectroscopy. The X-ray measurements were carried out on synchrotron radiation sources in England and California.

The connection with Alzheimer’s is unclear

Whether and what connection there is between the existence of nanoparticles in Alzheimer’s plaques and the development or progression of the disease remains an open question for the time being. Lermyte believes it is very likely that the metal particles influence biochemical processes.

“It is known that metallic nanoparticles have the effect of a catalyst and promote certain reactions,” explains the chemist, “in addition, it is likely that the chemical reactions that lead to the formation of these metal nanoparticles also give rise to reactive oxygen species, which are toxic to the cells of the brain. ”These mechanisms now need to be researched in detail.

also read

Graphic of an Alzheimer's affected brain

Because some are now speculating whether the ingestion of too much copper or iron with food could be a risk factor for Alzheimer’s, Lermyte emphasizes that water-soluble copper and iron are naturally required in the brain and are involved in metabolic processes there.

However, there seems to be no reasonable reason for the existence of metallic copper and iron in the brain. The crucial question is rather: Why are the discovered nanoparticles formed? And could that be a cause or just an unimportant accompanying circumstance in Alzheimer’s?

The diagnosis could be possible earlier

Lermyte thinks it is conceivable that the findings of this research could result in the possibility of a very early diagnosis of Alzheimer’s disease.

If the metal particles were to form in a very early phase of Alzheimer’s disease, a correspondingly early diagnosis would be possible because the nanoparticles could be detected with a sensitive magnetic resonance tomograph. But would it even make sense to find out about this impending fate ten or twenty years before the first symptoms appear?

also read

Alzheimer

“I wouldn’t even want to know,” says Alzheimer’s researcher Mathias Jucker from the Hertie Institute for Clinical Brain Research at the University of Tübingen, “at least not as long as there are no effective drugs available that can actually prevent the disease.”

This drug could be a game changer

The antibodies approved as Alzheimer’s drugs in the USA in June 2021 could possibly be a “game changer”, says Jucker, “but on the one hand they are not yet approved in Germany. And on the other hand, this antibody can at best postpone the disease but not prevent it, but it is quite possible that there will be antibody drugs that work even better in the years to come. “

also read

Gehrin

When it comes to new insights into iron and copper, Jucker is reluctant. “Yes, that is a very interesting research result, but the plaques in Alzheimer’s brains are, as it were, the gravestones of the disease process. Hundreds of things can be found in them and then you still have a long way to go whether these substances played a role in the development of Alzheimer’s. ”

Jucker points out that conspicuously high concentrations of aluminum were detected in Alzheimer’s plaques as early as 30 years ago. And to date there is no convincing evidence that aluminum increases the risk of Alzheimer’s disease.

For Alzheimer’s researchers, there are now definitely new leads, new hypotheses and a lot of work. How quickly and whether useful knowledge will emerge from this is open. In basic research, you never know what will come out in the end.

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