Unfortunately, every year more and more people worldwide fall ill with Alzheimer’s disease or other forms of dementia. In 2016, there were already almost 2.0 million people affected in Germany, 10 million in Europe and 35.5 million worldwide. Unfortunately, the trend is rising, with 115 million cases of the disease predicted worldwide by 2050.

The fear of Alzheimer’s dementia is great, because until now this disease was considered incurable. There is still no effective drug, although the pharmaceutical industry has been working hard on it for a long time. The reason for this lies in the nature of the disease: it is now known that dementia is a generalised metabolic disease, which manifests itself in the central nervous system, i.e. in our brain. 

The good news, however, is that the US neurologist Dr. Dale Bredesen – after more than 30 years of intensive research – has shown that it is possible to prevent and cure Alzheimer’s dementia, at least as long as there is no overly advanced damage to certain nerve cells of the brain. According to his research findings, the causes of the disease are not only to be found in the genes, but our lifestyle is also decisive: undetected infections and chronic inflammation, long-term unhealthy nutrition or malnutrition, as well as exposure to certain toxins are essential factors that can trigger and also accelerate the disease.

Thus, dementia diseases such as Alzheimer’s disease would no longer be an unsolvable fate, as the disease is reversible through changes and adjustments in lifestyle. It is therefore also possible to protect oneself from dementia in a preventive way. Moreover, it has been shown in many dementia patients that the disease can be stopped or the course of the disease can even be reversed, even if one is in a slightly advanced stage. 

Since this great opportunity must be seized, the project Knowledge stops Dementia would like to give you the opportunity to find suitable contacts in the preventive and therapeutic field. On the following pages we have therefore started to list doctors, therapists and coaches who practice in the field of dementia prevention or dementia therapy. All the therapists mentioned work holistically and individually on the patient with basic pillars in nutrition therapy, exercise therapy and other holistic forms of therapy.  The identification and reduction of harmful substances and microbial loads is also part of the preventive as well as therapeutic approach, which is also particularly important in biological dentistry, for example. Please be aware, though, that the individual therapeutic approaches may vary and we cannot evaluate them in detail at this point.

In addition to the appropriate therapy, it is extremely important to treat dementia patients appropriately in everyday life, which can push relatives safely to their limits. It is therefore of particular concern to us to point out here projects and initiatives that offer dementia patients and in particular their relatives (and caregivers)  help and support, exchange of experience, special programs, but also to offer possible starting points and face-to-face counseling.. The first step has now been taken with the ‘Singing Hospitals’, but we are sure that more projects will follow in the near future!

Just have a look at our Webpage under ‚Links and Support’

We hope that we can help you!

The diagnosis of Alzheimer’s disease (AD) has challenged neurologists for many years. It’s difficult to determine if someone will develop AD in the future, if the actual cognitive deficit is due to AD or to other cause of dementia and it’s also difficult to predict the pace or speed of disease progression.

It is already known that Alzheimer’s pathological brain alterations (amyloid plaques and Tau-tangles) start long time before the appearance of clinical symptoms. We also know that lifestyle interventions are the only effective treatment to fight cognitive decline, especially when initiated in early stages of disease. That’s why, a test which could predict when the process starts and the rhythm of progression would be a useful tool in the clinical practice.

Many tests are nowadays available (see Diagnosis section for more information), but they are expensive and difficult to be used in the day by day clinic. They usually require brain image techniques that are either expensive and time consuming or invasive medical procedure like lumbar puncture – which is not free of adverse effects. 

Two new AD-tests have been developed within the last year and hope to finally bring ease and precision to the diagnosis of AD.

Published in Neurology in August 2019, a study presents a blood test that was able to measure the level of Aβ42/Aβ40 with high correspondence with amyloid PET status (brain image test). It showed that plasma Aβ42/Aβ40, especially when combined with age and ApoE4 status (see Genetics section for further information), accurately diagnoses brain amyloidosis and can be used to screen this pathological alteration in individuals with normal cognitive function, i.e., before presenting symptoms. It also showed that individuals with a negative amyloid PET scan and positive plasma Aβ42/Aβ40 are at increased risk for converting to amyloid PET-positive. Thus, the test could be used to screen individuals likely to present brain amyloid deposit and hence, at risk for AD. 

In another study published in Lancet Neurology in May 2020, the authors developed and validated an ultrasensitive blood immunoassay for p-tau181. Tau phosphorylated at threonine 181 (p-tau181) level has been already measured in is cerebral spinal fluid (CSF) and is a highly specific biomarker for Alzheimer’s disease pathology. With this study, the authors showed that blood p-tau181 levels can predict tau and amyloid β pathological alterations and differentiate AD from other neurodegenerative disorders with high accuracy. Additionally, it predicts cognitive decline and hippocampal atrophy over a period of 1 year, making it suitable as a marker of disease progression.

Both tests have the advantage to be done in a blood sample, and were able to predict the risk of developing cognitive decline and its progression. They represent simple, practical and scalable tests for the diagnosis of AD. They are not yet available in the market, but have the potential to be incorporated into clinical practice as a rapid screening test to rule out AD and to guide therapy in patients with dementia. 

Considering the relevance of lifestyle measures for AD treatment and prevention, these tests provide security and certainty of when to start or intensify actions to control cognitive impairment. They can be also used to easily screen individuals at risk to future prevention trials, to promote lifestyle intervention and to improve our knowledge about this challenging disease.


Two  new tests for Alzheimer’s disease that determine highly specific biomarker substances in the blood, have been developed. These fast, precise and inexpensive tests may have important clinical applications: as a screening tool in the primary care setting; to monitor the disease progression; to differentiate AD patients from patients with other neurodegenerative disorders; and as a way of ensuring that subjects enrolled in clinical trials indeed have Alzheimer’s disease and that the treatments they are testing are effective. They will certainly become an important tool to ensure an accurate and early diagnosis and to motivate doctors and patients to implement lifestyle changes in order to prevent cognitive deterioration. KsD will keep its readers informed about the availability of these or other tests (please register today for our newsfeed).


  1. Karikari TK, Pascoal TA, Ashton NJ, et al. Blood phosphorylated tau 181 as a biomarker for Alzheimer’s disease: a diagnostic performance and prediction modelling study using data from four prospective cohorts. Lancet Neurol. 2020;19(5):422-433. doi:10.1016/S1474-4422(20)30071-5. https://pubmed.ncbi.nlm.nih.gov/32333900/
  2. Schindler SE, Bollinger JG, Ovod V, et al. High-precision plasma β-amyloid 42/40 predicts current and future brain amyloidosis. Neurology. 2019;93(17):e1647-e1659. doi:10.1212/WNL.0000000000008081 https://pubmed.ncbi.nlm.nih.gov/31371569/
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Although scientists have known for a long time that apolipoprotein E4 is a leading genetic risk factor for Alzheimer’s disease, it has long been unknown how exactly it leads to memory loss. US researchers now believe they have an answer. 

The gene Apolipoprotein E (ApoE) encodes an important lipid carrier protein in the brain, which is present in three different variants: ApoE2, ApoE3 and ApoE4. As with almost all genes, humans carry two copies of ApoE, which can be either the same or different variants. Compared to the most common ApoE3 variant, ApoE4 significantly increases the risk of Alzheimer’s: it is 4-fold higher in people with one copy of ApoE4 and up to 15-fold higher in people with two copies of this variant. Alzheimer’s patients who carry ApoE4 are more likely to develop symptoms of the disease earlier than carriers of other variants of ApoE (1). Read more about this in the chapter ‘Genetics‘.

This so-called late-onset Alzheimer’s disease is the most common form of dementia and is characterized by the extracellular accumulation of misfolded amyloid-β (Aβ) and intracellular aggregation of Tau proteins to form neurofibrillary tissues in the brain. It was long thought that the ApoE4 gene variant favours Aβ and Tau accumulation and thus contributes to the faster onset of Alzheimer’s disease. However, it is now clear that other damaging processes also play a role. For example, changes in the blood-brain barrier (BBB) have been shown to be early markers of this neurodegenerative disease. The degree of BBB dysfunction correlates directly with the extent of cognitive impairment, but which factors are responsible for its degradation was previously unknown. There is, currently, growing evidence that ApoE4, the leading genetic risk factor for Alzheimer’s disease, is related to BBB degradation (2).

But what exactly happens to the BBB and how is this in turn related to ApoE4 and the Aβ and Tau accumulation? 

To fill this knowledge gap, the permeability of the BBB in healthy people and in patients with mild cognitive impairment was investigated and the results were correlated with their ApoE status. The researchers found that people who were cognitively healthy and carried either one or two copies of the ApoE4 variant had leaking BBBs in the hippocampus and parahippocampus – brain regions that play a role in memory formation and are involved in learning processes. This leaky BBB was more pronounced in ApoE4 carriers who suffered from a slight cognitive decline. In contrast, the BBB was intact in cognitively healthy ApoE3 carriers;  But ApoE3 carriers who already showed cognitive impairment, presented also a leaky BBB.. Remarkably, these effects preceded all signs of tissue loss in  affected brain regions, confirming that BBB dysfunction is a very early event in the onset of neurodegeneration, meaning that the integrity of this important barrier is lost before cognition weakens (3).

Follow-up studies have shown that BBB damage in ApoE4 carriers is associated with pericyte degeneration (2). Pericytes border on the endothelial cells are cells of the inner walls of the blood vessels, and thus protect the brain capillaries. They normally maintain the integrity of the BBB by preventing the breakdown of the connections between endothelial cells that make up the capillary walls (3).  Pericyte destruction observed in ApoE4 carriers was independent of the accumulation of Aβ and Tau (2).

The mechanism of pericyte damage is now also known: these cells secrete the ApoE4 protein, which activates the protein cyclophilin A (CypA). This triggers a downstream signaling pathway that involves the activation of the inflammatory protein matrix metalloproteinase-9 (MMP9) in pericytes and possibly also in endothelial cells (4). This leads to an interruption of the connections between adjacent endothelial cells, which ultimately results in the disruption of the BBB in the hippocampus and parahippocampus. This mechanism is illustrated in the following figure (modified after Ref. 4):

Illustration Gen

These observations thus shed new light on ApoE4, and contradicts the widely held idea that this gene variant contributes to Alzheimer’s disease simply by promoting Aβ and Tau accumulation. 

Instead, the malfunctioning of the BBB seems to be responsible for the fact that ApoE4 carriers are susceptible to Alzheimer’s disease. This would also explain why ApoE4 carriers have a worse prognosis after a stroke or craniocerebral trauma than carriers of other ApoE variants (5). 

Interestingly, these early mechanisms that trigger the cognitive impairment seem to be different among  ApoE4 and ApoE3 carriers. It is possible that activation of the CypA pathway and damage to pericytes in ApoE3 carriers are not  involved in cognitive impairment. However, it remains unclear, whether a leaking BBB caused by pericyte-independent factors such as endothelial cell damage by Aβ (6) contributes to cognitive impairment in ApoE3 carriers . Many other questions also remain unanswered, such as whether and how BBB degradation directly leads to cognitive impairment, or whether it is a cause or a consequence of the disease process. The role of the BBB in ApoE2 carriers, which was not investigated in the present study, is also still unknown. But the research results shed more light on understanding the role of the ApoE4 gene. It may be possible to diagnose people  with the ApoE4 gene at an early stage  by examining the brain vessels, and individualized   therapy approaches could be taken early to effectively counteract premature cognitive decline. 


Damage to the pericytes that protectively surround the brain capillaries and seal the blood-brain barrier leads to a decline in cognition. In people with the gene variant ApoE4, this breakdown of the blood-brain barrier appears to be accelerated via an inflammatory pathway. This damage to the brain capillaries occurs at a very early stage, even before the tissue loss in the hippocampus occurs and cognition decreases. These new findings may offer the chance of early diagnosis in high-risk patients via the brain vessels, which is a promising approach in the fight against premature cognitive decline.Furthermore, they reinforce that the breakdown of the blood-brain barrier is the triggering mechanism in the pathophysiology of Alzheimer’s disease, being the accumulation of  Aβ  and Tau, secondary events.  


  1. Yamazaki, Y., Zhao, N., Caulfield, T. R., Liu, C.-C. & Bu, G. (2019): Apolipoprotein E and Alzheimer disease: pathobiology and targeting strategies. Nature Rev. Neurol. 15, 501–518
  2. Montagne, A. et al. (2020): ApoE4 leads to blood–brain barrier dysfunction predicting cognitive decline. Nature 581, 71–76
  3. Profaci, C. P., Munji, R. N., Pulido, R. S. & Daneman, R. (2020): The blood–brain barrier in health and disease: Important unanswered questions. J. Exp. Med. 217, e20190062
  4. Ishii, M. & Iadecola, C. (2020): Lipid carrier breaks barrier in Alzheimer’s disease. Nature 581, 31-3
  5. Mahley, R. W., Weisgraber, K. H. & Huang, Y. (2006): Apolipoprotein E4: A causative factor and therapeutic target in neuropathology, including Alzheimer’s disease. Proc. Natl Acad. Sci. USA 103, 5644–5651
  6. Cortes-Canteli, M. & Iadecola (2020): Alzheimer’s Disease and Vascular Aging  C. J. Am. Coll. Cardiol. 75, 942–951
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You go to a doctor – usually a neurologist – ask about natural or lifestyle-oriented therapeutic methods for dementia – and you often look into blank eyes, at worst into an aggressively wrinkled forehead “Don’t give me that, all dangerous nonsense, there are only a few pharmacological approaches that may really work!” 

In your journey of self-directed prevention and treatment of cognitive impairment and dementia you will often, probably even frequently, encounter this incredible narrow-mindedness among many medical doctors who question lifestyle-related causes and risk factors, and denigrate a causal therapeutic approach based on changes in lifestyle, the supply of vital resources and the reduction of pollutants as a story from the “realm of fantasy”. Hopefully you have not experienced it personally. 

How do you deal with it? You try to inform yourself more broadly, for example via the websites of Kompetenz statt Demenz, but of course you may still wonder, where is the evidence?


For this reason, we have provided a selection of current studies and reviews on the page “Alzheimer Research” and listed them chronologically together with the conclusions drawn by the authors. The studies listed there clearly show that targeted interventions, whether with micronutrients, sport and exercise, sleep hygiene or mental measures, may indeed help to regain lost cognitive abilities. They thus provide you with an important support for your argumentation on your difficult way through the narrow-mindedness and helplessness of the conventional medicine. The studies are sorted by category and the most recent studies are listed first. 

Intervention studies – also double-blind placebo-controlled – are the most interesting ones, as they directly assess the effects of a treatment. However, it does not always have to be a double-blind placebo-controlled study, because effects become visible even without blinding and some interventions cannot be blinded by the authors anyway (e.g. in the area of movement or mental interventions). 

Meta-analyses are interesting in the sense that they “pool” several or even many individual studies. However, the “pooling” of several studies is difficult and can contain statistical errors, and the selection of studies can also exhibit a “bias” (systematic error). A positive result of a metastudy at least provides additional safety. 

Reviews are also very helpful, as they look at a topic from an overview perspective and summarise it.

So if you are interested in a brief overview of the background of different therapeutic approaches and their scientific background, just go to this page: Alzheimer Research

You will also find direct links to the studies on Pubmed and some are also available free-of-charge in the full version. If you want to print the whole thing to go, just click on the right mouse button and “Print” and you will get the page in a quite clear print format.

A final note: Science never makes absolute statements “ex cathedra” but reflects the state of current research. Studies may be incorrect or even manipulated and their content may be overtaken by new findings. Therefore it is important to stay up to date and we at “Kompetenz statt Demenz” continuously follow up the relevant topics. For this reason, the most recent studies always come first and some may disappear from the list over time, but this is the sign of the further development of scientific knowledge.

Conclusion: Don’t let yourself be confused on your own path of self-responsible treatment and prevention of dementia and make up your own mind as much as possible! Use reliable sources of information to support your decision for any type of treatment and do not allow yourself to be discouraged. We at ‘Kompetenz statt Demenz’ hope to make our contribution!

PS: And if you happen to come across an important paper, please send us the link!

Photo by Michael Longmire on Unsplash

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A study published in The American Journal of Medicine 2018, has demonstrated that maintaining a healthy diet in midlife is independently associated with a larger hippocampus years later and may protect against cognitive decline. The hippocampus is a structure located in the temporal lobe of each brain hemisphere and is directly involved in the process of memory. The volume of the hippocampus can be determined by brain magnetic resonance imaging (MRI). Decreasing of its volume is related to cognitive impairment and is used in clinical practice for the diagnosis of Alzheimer’s disease (hippocampus atrophy).

MRI Brain Diet

In this study, the quality of the diet of 459 participants (average age at baseline = 49 years) was assessed with a food-frequency questionnaire, which was administered in 1991-1993 and 11 years later, in 2002-2004. At the end of the follow up, around 13 years after the first questionnaire, participants underwent brain MRI with study of the hippocampus. Long-term healthy diet (showed by higher cumulative score on the Alternative Healthy Eating Index), was associated with a larger total hippocampus volume. This association was independent of sociodemographic factors, smoking habits, physical activity, cardiometabolic factors, cognitive impairment, and depressive symptoms and was more pronounced in the left hippocampus than in the right hippocampus.

A healthy diet, based on recommendations in the Alternative Healthy Eating Index 2010 (AHEI-2010) score is rich in vegetables, fruits, whole grains, nuts, legumes, omega-3 fats, and polyunsaturated fatty acids, and is light on sugar-sweetened drinks, red and processed meat, trans fat, and sodium-rich products. It is also characterized by low alcohol intake. 

The findings of this study support the hypothesis that overall diet may affect brain structures with a specific impact on hippocampus volume. 

Some other studies have demonstrated the influence of diet in brain structures. In most of these studies, diet quality was assessed by Mediterranean diet score, and higher scores (healthier diet) were found to be associated with larger cortical thickness, lower white matter hyperintensity burden, and preserved white matter microstructure. All these findings indicate better preservation of normal brain structure. 

Another previous study, published in 2015 in the BMC Medicine, had already shown that higher intakes of unhealthy foods, normally present in the Western diet, were independently associated with smaller hippocampal volume. This finding was originally observed on experimental animal models and suggested that a high-energy diet rich in saturated fats and refined sugars adversely affect neuronal plasticity and function. Animals maintained on a high-energy diet rich in fat and sugar showed lower performances in hippocampus-dependent spatial learning, object recognition, reduced hippocampus levels of brain-derived neurotrophic factor (BDNF) and impaired in blood-brain barrier integrity.

Accounting for the importance of hippocampus with long-term, declarative, episodic memory, as well as for flexible cognition network, this study reaffirms the need to recognize diet and nutrition as potential determinants of cognition, mental health and social behavior.


A Long-term healthy diet (and not various episodic restrictive diets) is the key to promote brain health and prevent dementia.

Thus, routine dietary counseling as part of a doctor’s office visit is very important at a patient’s level, but it should also be a high-priority public health goal.

To know more: https://kompetenz-statt-demenz.de/en/prevention-treatment/nutrition/the-mind-diet/

  1. Akbaraly, T et al. Association of Long-Term Diet Quality with Hippocampal Volume: Longitudinal Cohort Study. The American Journal of Medicine 2018 https://www.ncbi.nlm.nih.gov/pubmed/30056104
  2. Gu Y, Brickman AM, Stern Y, et al. Mediterranean diet and brain structure in a multiethnic elderly cohort. Neurology 2015;85 (20):1744–1751. https://www.ncbi.nlm.nih.gov/pubmed/26491085
  3. Mosconi L, Murray J, Tsui WH, et al. Mediterranean diet and magnetic resonance imaging-assessed brain atrophy in cognitively normal individuals at risk for Alzheimer’s disease. J Prev Alzheimers Dis. 2014;1(1):23–32.https://www.ncbi.nlm.nih.gov/pubmed/25237654
  4. Staubo SC, Aakre JA, Vemuri P, et al. Mediterranean diet, micronutrients and macronutrients, and MRI measures of cortical thickness. Alzheimers Dement. 2017;13(2):168-177. https://www.ncbi.nlm.nih.gov/pubmed/27461490
  5. Jacka, F.N, Cherbuin, N, Anstey, KJ et al. Western diet is associated with a smaller hippocampus:a longitudinal investigation. BMJ 2015; 13:215 https://www.ncbi.nlm.nih.gov/pubmed/26349802
  6. Stranahan AM, Norman ED, Lee K, et al. Diet-induced insulin resistance impairs hippocampal synaptic plasticity and cognition in middleaged rats. Hippocampus. 2008;18(11):1085–1088. https://www.ncbi.nlm.nih.gov/pubmed/18651634
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The American researcher Dr. Pat McGeer investigated whether viruses could possibly cause the changes in brain cells which are  typical of dementia. He stained brain cells of patients who died with AD using a different staining method. Although he found no evidence of a virus, he found vast amounts of certain brain cells (so-called microglia). These cells only appear in such big amount under  one condition: inflammation! Dr. McGeer also found that microglia had already been discovered in the brain of dementia patients back in 1919. Although this theory was not further investigated at that time, it is currently receiving new attention.

In 2004, Dr. Scott Little and his colleagues investigated whether certain bacteria (e.g. chlamydia) might also be possible causes of AD. Dr. Scott and his team had already isolated chlamydia from nine out of ten AD patient brains. In subsequent animal experiments, it was shown that chlamydia can remain in the brain undisturbed by the immune system. Even after three months, the bacteria were still detectable in the animal brains. The researchers were also able to detect certain protein deposits. These deposits were larger and more frequent the more Chlamydia has spread in the brain.

US researcher Herbert Allen has also put forward the hypothesis that bacteria adhere to surfaces as biofilms and are therefore largely resistant to immune attacks or antibiotics. This prompted him to ask whether bacterial biofilms might also play a role in Alzheimer’s disease. When Allen searched for biofilms in the brains of deceased Alzheimer’s patients, he found them at the same sites in the hippocampus as the amyloid plaques. The key factor of innate immunity (the so-called toll-like receptor 2,TLR2) was also present in the same region of the Alzheimer’s brain, but not in the healthy controls. The researcher concluded that TLR2 is activated by the presence of bacteria but is blocked by the bacterial biofilm and instead the surrounding tissue is damaged.

These investigations clearly show that not only  the presence of plaques in the brain is responsible for Alzheimer’s dementia, but infectious processes may also play an essential role.  The brain is highly protected by the blood-brain barrier, which controls the passage of molecules into and out of the brain. It is now known that a broad spectrum of pathogens such as viruses, bacteria, fungi and protozoa (animal unicellular organisms) can still gain access to the brain. 

More on this topic and a tabular overview can be found here…

Moreover, the research results further suggest that even if a brain infection with microorganisms is not the triggering event in the neuropathogenesis ending with Alzheimer’s disease, but merely an opportunistic spread of the pathogen to an already damaged organ, such infections may well aggravate or accelerate the course of the disease.

Moreover, the research results further suggest that even if a brain infection with microorganisms is not the triggering event in the neuropathogenesis ending with Alzheimer’s disease, but merely an opportunistic spread of the pathogen to an already damaged organ, such infections may well aggravate or accelerate the course of the disease.


The connections must, therefore, be multi-causal and it is important not to think in terms of pure repair mechanisms again or to put all energy and money into the medicinal dissolution of plaques, but to question what is causing and systemically so wrong that more and more people are obviously becoming ill. So the  correct question is therefore: what causes our body system to work so wrong that the regeneration of the brain areas is no longer possible?

The answer is largely hidden in our western lifestyle, and this website reports on this in detail.

You can also become active yourself by getting your immune system in shape. You can find some tips on how to do this in this interview with Prof. Spitz and pharmacist Gröber from March 2020!

Interview with Prof. Spit and Apothecary Gröber March 2020! (in German language only, pls use automatic subtitles in YouTube)

The main elements are: vitamin D, vitamin A, vitamin C, zinc and selenium


  1. Akiyama, H., Ikeda, K., Katoh, M., McGeer, E.G, McGeer, P.L. (1992):  Expression of MRP14, 27E10, interferon-α and leukocyte common antigen by reactive microglia in postmortem human brain tissue. Journal of Neuroimmunology 50/2, pp 195-201
  2. Little, C.S, Hammond, C.J., MacIntyre, A., Balin, B.J., Appelt, D.M. (2004): Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice. Neurobiology of Aging 25/4, pp 419-429
  3. Sochocka, M., Zwolinska, K., Leszek, J. (2017): The Infectious Etiology of Alzheimer’s Disease. Current Neuropharmacology, Volume 15, Number 7, pp. 996-1009(14)
  4. Allen, H.B. (2019): The essential role of biofilms in alzheimer’s disease. Microbiology & Infectious Diseases 3 (2), pp 1-3


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Although known to be essential for all animals with nervous system, the main cellular function of sleep is still unknown. Prolonged sleep deprivation can be lethal, and sleep disturbances are associated with various deficiencies in brain performance. 

Far from being relaxed when we’re sleeping, our brains are very active and uses a lot of energy. Most of the energy is spent on important “housekeeping work” such as: cleaning up, consolidating memories, getting rid of data it doesn’t need and cleaning out physical waste products, including beta-Amyloid deposits.

The mechanisms underlying solute clearance from the brain’s extracellular space have puzzled neurologists for centuries, once the central nervous system (CNS) is the only organ system lacking lymphatic vessels to assist in the removal of interstitial metabolic waste products. Recent studies have led to the discovery of the glymphatic system, a glial-dependent perivascular network with a lymphatic-like function in the brain.

The glymphatic pathway is a highly-organized fluid transport system where cerebrospinal fluid (CSF) and interstitial fluid (ISF) continuously interchange. In its initial segments, CSF from the subarachnoid space flows into the brain through perivascular spaces of the large arteries and is driven into the brain parenchyma through the perivascular spaces of penetrating arteries, also known as Virchow-Robins spaces. This flow across the brain parenchyma is facilitated from the water channels aquaporin 4 (AQP4), a protein which is densely expressed by glial cells. While flowing, the CSF mixes with the ISF. In the interstitium, the mixed fluid disperses via a polarized net fluid movement directed towards the venous perivascular space (fig1).

Potential factors affecting glymphatic pathways include respiratory cycle, arterial pulsations, changes in vasomotor tone, postural changes and sleep. This last factor is significantly important in cleaning waste product: the clearance of amyloid beta (Aß) during sleep is twice as fast as during awake periods.

Besides cleaning, the brain also needs sleep to replenish itself. During REM-stage and dreaming the brain works on fixing any damage suffered during the daytime: restores the metabolic stores, trims unneeded synapses, reinforces specific connections and overall becomes more energy efficient. It also works repairing damaged DNA inside neurons, increases chromosome dynamics and performs nuclear maintenance. These changes in chromatin dynamics have been shown to regulate key nuclear processes, including epigenetic functions.


The glymphatic system is a recent described mechanism that our brain uses to eliminate physical waste products, like amyloid beta (Aß). This system works mainly during sleep, specially during deep stages of sleep. This may help to explain the biological need for sleep across all species and reinforces the importance of a good night of sleep.

Sleep well and allow yourself to experience a proper brain “detox”, helping to prevent AD.


    1. Tarasoff-Conway JM, Carare RO, Osorio RS, et al. Clearance systems in the brain-implications for Alzheimer disease [published correction appears in Nat Rev Neurol. 2016 Apr;12(4):248]. Nat Rev Neurol. 2015;11(8):457–470. doi:10.1038/nrneurol.2015.119 https://pubmed.ncbi.nlm.nih.gov/26195256/
    2. Zada, D., Bronshtein, I., Lerer-Goldshtein, T. et al. Sleep increases chromosome dynamics to enable reduction of accumulating DNA damage in single neurons. Nat Commun 10, 895 (2019) doi:10.1038/s41467-019-08806-w https://pubmed.ncbi.nlm.nih.gov/30837464/
    3. Rasmussen MK, Mestre H, Nedergaard M. The glymphatic pathway in neurological disorders. Lancet Neurol. 2018;17(11):1016–1024. doi:10.1016/S1474-4422(18)30318-1 https://pubmed.ncbi.nlm.nih.gov/28466758/
    4. Jessen NA, Munk AS, Lundgaard I, Nedergaard M. The Glymphatic System: A Beginner’s Guide. Neurochem Res. 2015;40(12):2583–2599. doi:10.1007/s11064-015-1581-6 https://pubmed.ncbi.nlm.nih.gov/30480554/

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This descriptive documentation of the Arte TV channel shows very clearly the connections between an unbalanced diet, the resulting micronutrient deficiencies and the effects on the brain. Various experiments have shown that mice that grow up with a deficiency of omega-3 fatty acids have deficits in the formation of their neurons and are much more anxious.

A particularly striking example showed an experiment with field hamsters. Here a simple vitamin B3 deficiency was sufficient to trigger aggressive behaviour during mating in over 80% of females. In the further course of the experiment, these females even ate their offspring directly after birth. After the vitamin B3 deficiency had been remedied, the females showed normal behaviour again, despite continued unbalanced diet  (thus the vitamin B3 factor could be clearly identified as the trigger).

In humans, long-term observations and studies showed similar results. Already in the uterus, the nutrition of the mother decides about the brain development and the emotional development of the fetus and newborn.

Mothers who eat “junk food” with a low omega-3 fatty acid concentration and high sugar content give birth to children that tend to act more aggressive. If this form of nutrition is continued in childhood, aggressive  behaviour, anxiety and attention disorders are pre-programmed. If there is a lack of omega-3 fatty acids, the function of the brain is disturbed, the communication between neurons and the neurogenesis are impaired.

The second cardinal error of Western nutrition is the flooding of highly processed foods with cheap refined sugars. Experiments have shown that this hidden sugar poisoning may show higher addiction effects  than cocaine. The consequences are insulin resistance, diabetes and dementia.

Of course, this form of unbalanced nutrition also has an effect on the intestines and the gut microbiota (and their genetic diversity, the microbiome), which have a significant influence on the health of our body and mind. Concrete examples show that the density of nutrients in food influences the way we   make decisions and solve daily problems. But we do not want to reveal too much here, watch for yourself:


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Unfortunately this excellent video don’t provide English subtitles, a more scientific alternative about the MIND diet in English can be found here:


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As far as mental and brain health is concerned, nutrition seems to be a major component of prevention, particularly with regard to dementia.  An alteration towards the Mediterranean diet or even better the MIND diet  increases our chances to remember the names of our grandchildren in the future and to actively participate in life. Just leave the “industrial garbage” on the shelf, even if it is sometimes difficult.

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The association between cognitive function and oral health has been well documented so far by some observational studies. On the one hand it has been reported that periodontal disease and tooth loss are associated with increased risk of dementia. On the other hand, improved memory after dental intervention has also  been observed. 

Those findings started the discussion about what would come first: Does initial cognitive decline lead to poor oral hygiene and dental loss, followed by poor nutrition, including decreased intake of vitamins, which would precipitate dementia? Or does periodontal disease increase concentrations of circulating inflammatory markers that might be involved in the pathogenesis of dementia?

Recently, this relationship has become clearer, with the characterization of Amyloid β (Aβ) as an antimicrobial peptide. Chronic periodontitis and infection with Porphyromonas gingivalis – a keystone pathogen in the development of chronic periodontitis – are significant risk factors for developing Aβ-plaques, dementia and AD. 

In a study published in Science Advances (1), a multinational team of investigators found that the presence of oral P gingivalis infection in mice resulted in brain infiltration by the bacteria, what was followed by increased production of Aβ, the component of amyloid plaques implicated in AD. They also found that AD brains showed a greater immunoreactivity to gingipains – a virulence factor produced by P gingivalis – than brains of non-AD control groups . Moreover, DNA from P gingivalis was found in the cerebral spinal fluid (CSF) of living AD patients and in postmortem studies of AD patients.

These findings offer evidence that brain infection with P gingivalis is not a result of poor dental care following the onset of dementia or a consequence of late-stage disease, but an early event that can explain the pathology found in middle aged individuals before cognitive decline. 

It supports the concept that Aβ is an antimicrobial peptide and reinforces the importance of maintaining a healthy microbiome to prevent AD.

Once the oral cavity is infected, P gingivalis may access the brain via a number of pathways including: 1) infection of monocytes followed by brain recruitment, 2) direct infection and damage to endothelial cells protecting the blood-brain barrier, and/or 3) infection and spreading through cranial nerves [e.g., olfactory or trigeminal] to the brain. 

After entering the brain, it modulates inflammatory innate and adaptive immune responses and activates the Aβ inflammatory cascade (see section causes for further information) with production of Aβ-plaques

Treating chronic periodontitis and P gingivalis infection with antibiotics or using a gingipain inhibitor could reduce the inflammatory response and brake Aβ-plaques formation. But the whole problem would reappear in case of a new episode of P gingivalis infection. 


The most important factor here is to keep a strong and healthy oral microbiome, which can prevent dysbiosis and assure the balance of oral cavity immune system. Who would have thought that a clean toothbrush and a proper oral hygiene (without too much fluoride) helps to stay mentally fit?


Dominy SS, Lynch C, Ermini F, et al. Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors. Sci Adv. 2019;5(1):eaau3333. https://www.ncbi.nlm.nih.gov/pubmed/30746447

Yamamoto T, Kondo K, Hirai H, et al. Association between self-reported dental health status and onset of dementia: a 4-year prospective cohort study of older Japanese adults from the Aichi Gerontological Evaluation Study (AGES) Project. Psychosom Med 2012; April 74 (3): 241-8 https://www.ncbi.nlm.nih.gov/pubmed/22408130

Wu B, Fillenbaum GG, Plassman BL, Guo L. Association Between Oral Health and Cognitive Status: A Systematic Review [published correction appears in J Am Geriatr Soc. 2016 Aug;64(8):1752]. J Am Geriatr Soc. 2016;64(4):739–751. https://www.ncbi.nlm.nih.gov/pubmed/27037761

Harding A, Robinson S, Crean S, Singhrao SK. Can better management of periodontal disease delay the onset and progression of Alzheimer’s disease? J Alzheimers Dis. 2017; 58 (2):337-348 https://www.ncbi.nlm.nih.gov/pubmed/28453484

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The focus of Alzheimer’s research has been, so far, the molecular process which leads to a change in the brain structure, above all and first in the hippocampus. Here, an increased formation of  amyloid beta (Aß) plaques is observed in the brains of Alzheimer patients. These protein adhesions impair the communication between nerve cells. Such alterations are attributed to ageing and genetic predisposition. As a result, Alzheimer’s research has been searching for years (but without any success) for a drug therapy to eliminate or at least reduce plaque formation. A very monocausal view of the problem.

Thus there are also studies suggesting that plaque formation cannot be the only underlying problem, since there are certainly old people with strongly increased plaque formation who are mentally extremely fit. 

Dementia researcher David Snowdon at the University of Minnesota made an impressive study questioning plaque formation as a monocausal cause in the so-called nun study, in which a total of 678 nuns aged between 76 and 106 participated.

Since 1986 Snowden was allowed to test the mental abilities of the nuns and after their death to examine the brains for signs of dementia. The astonishing result: Some brains of nuns who were mentally fit and active up to old age and had an excellent memory, all had “plaques” like in a severe Alzheimer’s dementia. 

Subsequently and in parallel, other influencing factors were intensively investigated. These included viral and bacterial infections, but most of all chronic inflammations.  In addition, there is the problem of insulin resistance caused by excessive sugar consumption by the population in industrialized countries. Today, it is very likely that Alzheimer’s disease is based not only on genetic factors but also on negative lifestyle factors that promote chronic inflammation and insulin resistance of brain cells. Some doctors even refer to Alzheimer’s disease as type 3 diabetes. Amyloid-ß plaques, on the other hand, are a natural protective mechanism that intents to ensure that no more brain cells perish! They are therefore a warning signal, but not a cause.

You can find detailed considerations on the scientific basics and the cause research here….

At the same time, however, this is a bridge to meaningful Alzheimer’s prevention and treatment. A reduction and avoidance of insulin resistance as well as an anti-inflammatory diet and way of life, among other things by:

If you implement these points widely, your Alzheimer’s risk will drop drastically.

In a study conducted by the University of Leipzig, scientists have identified the potential for preventing Alzheimer’s dementia in Germany. Based on internationally available study results, seven risk factors were specifically investigated: High blood pressure, obesity in middle age, depression, physical inactivity, smoking and low education.  The result: about 50% of dementia cases could be avoided by preventive measures alone regarding these risk factors!

Conclusion: Even if the available numbers correspond to theoretical projections, the vast potential for prevention can still be presumed. Especially in the context of demographic change and the corresponding ageing of the German population, preventive measures and educational programmes on Alzheimer’s dementia such as the KsD project are becoming increasingly important.


[1]  Luck, T. & Riedel-Heller, S.G. Nervenarzt (2016) 87: 1194. https://doi.org/10.1007/s00115-015-0045-1

Photo: Maria Teneva

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