Ashwagandha (Withania somnifera), also known as Indian ginseng or Winter cherry, is one of the most important herbs in Ayurvedic medicine. It has been used for millennia as a rejuvenating tonic, i.e. to increase physical and mental health by promoting longevity. Classically, different parts of the plant (including roots, leaves and flowers) have been used to treat different conditions such as rheumatism, constipation, insomnia, chronic stress and hormonal imbalances.

Recently, the benefits of this herb have aroused the interest of conventional western medicine and in the last 10 years many studies have been published bringing scientific evidence for what the ancients used to practice many years ago.

Although studies in humans are still limited, both in vitro and animal model research shows evidence of Ashwagandha’s effect on the treatment of diabetes, cancer, stress, anxiety, schizophrenia, male infertility, neurodegenerative diseases, as well as on muscle mass gain and athlete performance.

Most of Ashwagandha’s effects are attributed to its ability to regulate hormone secretion and to adapt the body to stress. It is, therefore, considered a strong adaptogen. Its main action is to balance cortisol, a hormone secreted by the adrenal gland in situations of prolonged stress. However, other effects have already been reported, including anti-inflammatory and antioxidant effects.

Ashwagandha also reduces the level of amyloid beta (Aβ) deposits in brain cells and promotes regeneration of the axon (part of the nerve cell involved in nerve impulse transmission). Such effects show a possible role for this herb in the treatment of Alzheimer’s disease. In animal models we indeed can observe reversal of neuronal atrophy and recovery of synaptic function after treatment. Prevention of memory loss and improvement of dementia symptoms have also been reported.

Human studies are still rare, but there are reports of improved executive function, attention and information processing speed in patients with mild cognitive impairment – ICM (1) and bipolar disorder (2), in randomized clinical trials.

Ashwaganda’s mechanism of action in the treatment of Alzheimer’s disease was recently elucidated in an animal model study (3): rats with scopolamine-induced memory loss (a model widely used in studies for Alzheimer’s disease) showed recovery of symptoms after being fed with concentrated extract of W. somnifera leaf. In this study, the effects of Ashwagandha both in neuroprotection (nerve cell protection against lesion) and neurotrophism  (neuronal growth and regeneration) were well documented.

It was also demonstrated (4) that Ashwagandha’s effect on brain cortex functions occurs due to stimulation of acetylcholine receptors (M1 muscarinic receptors). Acetylcholine is an important neurotransmitter, acting as a promoter of the communication between neurons (synapse).  Stimulation of M1 receptors can mimic the effect of acetylcholine, improving nerve impulse transmission and reducing the symptoms of the disease.

The importance of acetylcholine in the physiopathology of Azheimer’s disease is so well established that one of the most common drugs for AD acts precisely by increasing the availability of this neurotransmitter in the brain. This group of drugs are called “cholinesterase inhibitors” (learn more at our section about  treatment).

Future clinical trials will bring more clarity about the effects of Ashwagandha on Alzheimer’s disease. Meanwhile, we count with the millenial use of Ashwagandha by tradicional systems of medicine being gradually confirmed by scientific studies of modern medicine.


Ashwagandha is a potent adaptogen, traditionally used in Ayurvedic medicine. Its effects on memory, cognition and longevity are well known. Current scientific studies have elucidated its mechanism of action proving its effectiveness and turning this ancient herb into a promising weapon for the prevention and treatment of Alzheimer’s disease.


  1. Choudhary D, Bhattacharyya S, Bose S. Efficacy and Safety of Ashwagandha (Withania somnifera (L.) Dunal) Root Extract in Improving Memory and Cognitive Functions. J Diet Suppl. 2017 Nov 2;14(6):599-612.
  2. Singh N, Bhalla M, de Jager P, Gilca M. An overview on ashwagandha: a Rasayana (rejuvenator) of Ayurveda. Afr J Tradit Complement Altern Med. 2011;8(5 Suppl):208-213. doi:10.4314/ajtcam.v8i5S.9
  3. Konar A, Shah N, Singh R, Saxena N, Kaul SC, Wadhwa R, Thakur MK. Protective role of Ashwagandha leaf extract and its component withanone on scopolamine-induced changes in the brain and brain-derived cells. PLoS One. 2011;6(11):e27265.
  4. Konar A, Gupta R, Shukla RK, Maloney B, Khanna VK, Wadhwa R, Lahiri DK, Thakur MK. M1 muscarinic receptor is a key target of neuroprotection, neuroregeneration and memory recovery by i-Extract from Withania somnifera. Sci Rep. 2019 Sep 30;9(1):13990.
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Can the course of early Alzheimer’s disease be delayed by consuming a special mixture of nutrients? This question was investigated in the European study called ‘LipiDiDiet’ led by Prof. Tobias Hartmann. 

The scientists recruited Alzheimer’s patients, who were in the early stages of the disease, to test the effectiveness of a specific nutritional drink called ‘Souvenaid’. Souvenaid was developed as a medical dietary food for the treatment of early-stage Alzheimer’s disease and is marketed by Nutricia (Danone Group). It contains a defined nutrient combination of long-chain omega-3 fatty acids, phospholipids, choline, B vitamins (B6, B12 and folic acid), vitamins C and E, selenium and uridine monophosphate. 

In this randomized double-blind study, the 311 participants were divided into two groups. The treatment group received the drink daily for breakfast. The control group was given daily  the same amount of a placebo drink, but with identical taste, consistency, color and calorie content. Neither patients, physicians nor researchers knew who was given the placebo or the multinutrient drink. 

The primary study endpoint was the slowing of cognitive decline. It was measured by a neuropsychological test battery, i.e., a combination of standardized cognitive testing procedures which measures not only the change in cognitive performance but also the ability to perform certain executive functions, such as planning, strategy and working memory. Furthermore, clinical aspects were also investigated using imaging techniques. Thus, structural brain changes could be directly recorded and assessed. 

Initial interim results after 24 months indicated some efficacy of the sip feed, but the differences in cognitive deterioration between the two patient groups were not significant. 

In September 2020, results after 36 months of treatment were published. They revealed significant differences between the two groups: Patients in the intervention group were measured to have 22 percent less brain atrophy, meaning that the brain mass of the treated Alzheimer’s patients had shrunk significantly less than that of the control group. Thus, the degenerative change process in the brain could be significantly slowed down by the nutrient preparation. In particular, the deterioration in the memory region of the brain (hippocampus), was 33 percent less in the treated patients than in the control group. It was also observed in regard to cognitive brain performance: it deteriorated 60 percent less, i.e. significantly less, in the treated subjects than in the no-treated patients.

Thus, the results of this study made it clear that such nutritional supplementation is not an effective concept in the short term. The effects seem to consolidate only with longer-term treatment, which was more than clearly shown by the comparison after 3 years with the interim results after 2 years. The researchers further found that the positive effects of the sip feed increased over the course of the treatment period and were not only focused on the memory region, but also extended to other cognitive areas. For example, the subjects were better able to cope with everyday challenges, such as paying bills, remembering routes, etc., than the control group.

This means that long-term intake of this specific multinutrient combination partially protects brain structures and reduces cognitive and functional decline in early Alzheimer’s disease. Thus, these nutrients appear to play a central role in reducing the neurodegenerative process in AD, suggesting a special nutritional need in AD. 

However, since it can be assumed that the disease begins decades before the first symptoms appear, but this cannot yet be measured with current methods, the timing to start therapy would also be crucial: the earlier, the better. Thus, not only the long-term duration of treatment would be important, but also the early start of treatment in the course of the disease. 

Despite intensive research, there is unfortunately still no medication that could cure Alzheimer’s disease. The currently available drugs can temporarily improve the symptoms, but let the patients fall back into the initial situation after some time. A sustained 3-year benefit of treatment, such as that achieved in this study with a defined nutrient mixture, has not yet been reported in incipient AD. With this in mind, the slower progression of the disease would already be a great success and is certainly a good start. 

These findings emphasize once again that AD is a generalized metabolic disorder in which monocausal therapies alone cannot lead to success, but multifactorial strategies must be used. And the international FINGER study (Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability) has already impressively demonstrated that multimodal prevention approaches can also pass clinical testing effectively. The ‘Souvenaid’ study is certainly a good start, as a sustained positive effect in terms of cognition, function and brain atrophy in an intervention for incipient Alzheimer’s disease has not yet been reported. Future studies could further clarify whether the efficacy of nutrient supplementation can be further enhanced if started at an even earlier stage, over a period longer than 3 years, as part of a multimodal intervention (e.g. FINGER trial) or in combination with pharmaceutical therapies.


The results of the aforementioned studies impressively underline that the multifactorial catalog of measures proposed by Knowledge stops Dementia – and especially a conscious diet that protects the brain – is the royal road in dementia prevention. It offers us a multitude of prevention strategies with which we can reduce our individual risk of Alzheimer’s disease by consistently minimizing avoidable risk factors and by adhering to a healthy lifestyle that includes not only nutrition but also other factors such as exercise, quality of sleep, social contacts, and so on. At the project ‘Knowledge stops Dementia’ you will find a lot more exciting and helpful information on this, so that you can maintain your mental health for as long as possible!


  1. Soininen H et al. (2017) 36-month LipiDiDiet multinutrient clinical trial in prodromal Alzheimer’s disease . Alzheimer’s and Dementia: 1-12 
  2. Soininen H et al. (2020) 24-month intervention with a specific mulitnutrient in people with predromal Alzheimer´s disease (LipiDiDiet): a randomised, double-blind, controlled trial. Lancet Neurol 16: 965–975 
  3. Ngandu T et al. (2015) A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial. Lancet 365: 2255–2263 
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With the project ‘Knowledge stops Dementia’, the Deutsche Stiftung für Gesundheitsinformation und Prävention, together with the Akademie für menschliche Medizin, presents a broad spectrum of measures to prevent the development of dementia. Within preventive measures, speech therapy offers an important therapeutic component that enables dementia patients to maintain contact with their environment. Especially in the early stages of the disease, no time should be lost and no one should hesitate to seek speech therapy treatment. 

A guest article by speech therapist Karen Grosstück from Hamburg

In the course of dementia, many people affected by the disease suffer from problems in finding words, often also problems in understanding complex texts. The change in communicative skills often makes the everyday life of patients and caregivers very difficult. It is a complicated situation for the people concerned and also represents a major challenge for the social environment. Difficulties in communication can affect the relationship between partners or family members and  in the course of time, can also complicate care and support.

If you search for the right word more and more often, you might ask yourself: am I just dizzy or is it already the beginning of dementia?

Difficulty in finding the right word does not necessarily mean the beginning of dementia, but there are typical language symptoms and communicative problems in Alzheimer’s dementia that occur early on. 

These include:

  • Affected persons digress in conversation, abruptly change the topic or prefer to stick to recurring topics
  • Those affected show less and less motivation to initiate conversations or to participate in conversations in everyday life
  • Expressions become increasingly lacking in content
  • Word-finding disorders make it difficult to formulate your own thoughts
  • Language comprehension problems lead to misunderstandings in daily life
  • Conversation contents are quickly forgotten

This is where speech therapy can help. Speech therapists support people with dementia in their ability to communicate and advise relatives in dealing sensitively with altered communication skills. 

What do speech therapists do? 

Speech therapy deals with disorders of speech, speaking, voice and swallowing in children and adults. Speech therapists determine whether such a disorder exists and know how to treat it. After a diagnosis, treatment and consultation follow with the aim of improving the quality of speech, language, voice and swallowing. Speech therapy is a medical remedy and can be performed on an outpatient basis, as prescribed by the physician, or as part of an inpatient treatment. 

What exactly can speech therapy do for people with dementia in particular?

In cases of dementia, speech therapy can cover both speech and swallowing. Logopaedic services should therefore maintain the communication and the nutritional situation, under changed conditions, in the best possible way. The treatment is always based on the everyday life of the person affected and takes into account his or her previous life as well as the current life context. Already at the beginning of the illness, logopedic consultation and preventive offers can help to prevent communication disorders. 

The prerequisite for contact with a person with dementia is an exclusively resource-oriented view. Since learning in the classical sense can no longer take place, it is necessary to discover new possible approaches and adequate them to the patient, in order to support and maintain the abilities as long as possible. The most important resource here is often nonverbal communication. Communicative skills such as facial expressions, gestures and speech melody can remain stable for a long time in Alzheimer’s disease. Thus, the important principle in conversation is: It is more important how something is said and less important what is said. Principles such as “the tone makes the music” and “relationship before content” characterize communication with a person with advanced dementia.

What are the goals of speech therapy for dementia?

  • The preservation of the highest possible communicative independence of the affected person
  • The participation of patients in social life
  • The best possible quality of life for the affected person as well as relief, support and advice for relatives

The earlier a person with dementia has the opportunity to express his or her language problems and work on them in a logopaedic therapy, the more he can benefit from it in the future. Especially at an early stage of the disease, many people try to hide their language deficits, hide word finding disorders and thus get into additional stress situations. Here it helps to be able to discuss the problems with a speech therapist in a protected setting. For many of those affected, it is important to write down their thoughts or biography at this early stage of the illness. Speech therapy can make it possible: it works with the emotional abilities and cognitive reserves of a person and uses the neuronal plasticity of the brain, which is still possible in the case of dementia. 

Where can you find more information and help?

Unfortunately, the benefits of early logopedic treatment for people with dementia are still not widely known. Often patients come to speech therapy too late and are no longer able to benefit from speech-activating treatment. Therefore, it is important to us to point out this largely unknown but extremely effective therapeutic option in the course of the project Knowledge stops Dementia. You can find out more about the topics covered by speech therapy, the methods used in speech therapy, how swallowing can be supported and much more in the brochure ‘Speech Therapy and Dementia’ by the Arbeitskreis Logopädie Demenz Hamburg in cooperation with the Alzheimer Gesellschaft/ Kompetenzzentrum Demenz Schleswig-Holstein. 

Current addresses of speech therapy practices in your area with a focus on dementia treatment can be found at and on our website under Knowledge stops Dementia

To the author:

Karen Grosstück works as a speech therapist with a focus on neurological speech and language therapy. She runs a private practice for speech therapy and nutrition in Hamburg. Further information can be found here.

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The fact that our health begins in the gut has been known for thousands of years. Today it is clear that our intestines are more than just a “digestive tube”, as this important organ fulfils a variety of other functions. For example, a disturbance of gut health is directly related to the development of chronic diseases.

 The intestinal flora, i.e. the microbial colonization of the intestinal mucosa, plays a particularly important role in this process. The intestinal flora is also known as the ‘intestinal microbiota’. It is the most important part of our immune system and thus offers us effective protection against infection.

But what few people know is that a correctly composed intestinal flora is also essential for our brain health, as it is directly connected to our nervous system via the intestinal-brain axis. An imbalance in the intestinal flora can lead to devastating consequences for the nerve tissue and in the worst case can cause neurodegeneration and dementia.

Alterations in the composition of the gut microbiota, caused by dietary changes, antibiotic exposure, and infection lead to the loss of the physiologic balance, which is implicated in the development of several diseases in humans, including Alzheimer’s disease. Recent evidence points to a causative link between changes in the intestinal microbiota composition, along with inflammatory changes in brain tissue. Hence, gut microbes may alter the level of neurotransmitter-related metabolites, affecting gut-to-brain communication and/or altering brain function.

Many studies on animal models have provided strong evidence of the importance of microbiota in the pathology of Alzheimer’s disease. Interesting results have been obtained, for example, with mice reared without intestinal microbial colonization and therefore without intestinal microbiota. These ‘aseptic’ mice showed an increased permeability of the blood-brain barrier (BBB) compared to mice with normal intestinal flora. This means that pathogens and other harmful substances from which the brain with an intact BBB is normally protected, are now able to enter the brain tissue. This can lead to an inflammatory reaction in the central nervous system called neuroinflammation, which is directly linked to the development of Alzheimer’s disease (see section causes for further information).

Such results obtained in animal models have also been confirmed by clinical studies:  For example, the intestinal microbiota of elderly people suffering from cognitive disorders was investigated, and an association between plaque deposits in the brain with the occurrence of pro-inflammatory intestinal bacteria and other inflammation markers could be shown.

In summary, all these results provide clear evidence that the effect of the intestinal microbiota on the development of the amyloid pathology may be significant and thus define its important role in the pathogenesis of Alzheimer’s disease.

But the good news is that our gut microbiota is a dynamically modifiable system that is very sensitive to lifestyle and ageing. With this knowledge, we can use a healthy lifestyle to positively influence our intestinal microbiota and develop practical recommendations for the prevention and treatment of Alzheimer’s disease.

Are you curious and would like to know more about this topic? 

To support the project ‘Knowledge stops Dementia’ ( the Academy of Human Medicine (AMM) has developed a fact sheet on dementia and intestinal health, which provides you with an evidence-based but compact overview of the above described relationships.

If you are interested in this fact sheet, it would be best to take part in the AMM’s current fundraising campaign for KSD.

Click here for the current AMM fundraising campaign… 

And don’t forget: healthy gut, healthy brain!

We thank you in advance for your support!

Your KsD team


  1. Vogt NM, Kerby RL, Dill-McFarland KA, et al. Gut microbiome alterations in Alzheimer’s disease. Sci Rep. 2017;7(1):13537.
  2. Harach T, Marungruang N, et al.  Reduction of Abeta amyloid pathology in APPPS1 transgenic mice in the absence of gut microbiota. Sci Rep. 2017 Feb 8;7:41802. 
  3. Kowalski K, Mulak A. Brain-Gut-Microbiota Axis in Alzheimer’s Disease. J Neurogastroenterol Motil. 2019;25(1):48‐60. 
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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!

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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Lithium is probably best known as a treatment for bipolar disorder but a very small dose of this element has been recently studied to prevent and slow the progress of AD. However, effective doses can sometimes cause negative side effects. 

Using animal models, scientists from McGill University (Canada) are now suggesting a novel microdose formulation of lithium could not only slow the progression of AD, but also potentially improve cognition at the early stages of decline. They tested a therapeutic agent called NP03, an encapsulated oral lithium formulation that can bypass degradation by acids in the gastrointestinal tract, resulting in high central nervous system uptake. This means significantly lower doses can be administered compared to conventional lithium.

The first study was published in 2017 and established the efficacy of the new microdose lithium formulation in the early or preclinical stages of AD by ß-Amyloid (Aß) deposition and restoring hippocampal neurogenesis. 

Microdoses of lithium at concentrations hundreds of times lower than applied in the clinic for mood disorders were administered at early amyloid pathology stages in the Alzheimer’s-like transgenic rat. Remarkably positive results of this study stimulated the researches to continue working and testing the new formulation on a more advanced pathology.

The new study explores the effects of the microdose formulation of lithium (NP03) on a slightly more advanced stage of AD, when amyloid protein plaques have begun forming and symptomatic signs of cognitive decline are already present. The results impressively demonstrated that NP03 reduced levels of amyloid plaques, reversed memory deficits, and lowered neuroinflammatory markers in the rodent model.

These results point to the potential neuroprotective benefits from sustained lithium microdoses and offer hope for AD treatment. However, it is important to note this particular microdose formulation is still yet to be tested in human subjects with AD, so much more work is necessary before it can be deployed as a clinical treatment.

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Lanabecestat is a potent inhibitor of Amyloid beta (Aβ) formation – the main component of amyloid plaques. Aβ is formed through cleavage of amyloid precursor protein (APP) by proteases known as secretases (β and γ). The Beta-site-APP-cleaving enzyme 1 (BACE1) cleaves APP at the β-secretase site, after which APP is cleaved by γ secretase to generate Aβ peptides. Lanabecestat inhibits BACE1 and was able to reduce levels of Aβ1-40 and Aβ1-42 in the brain, cerebrospinal fluid (CSF), and plasma in several animal models, as well as in human CSF and plasma. Besides that, Lanabecestat is brain permeable meaning that an adequate amount of this substance is able to reach the brain after oral intake.

Taking these facts into account, two clinical trials were designed to test if the oral administration of Lanabecestat would be effective in two different groups of patients: patients with mild cognitive impairment (the AMARANTH study) and patients with mild AD (the DAYBREAK-ALZ study). The main question in both studies was: can Lanabecestat slow the progression of cognitive deterioration?

Unfortunately, both studies had to be earlier terminated because no benefits were found in the groups using the substance compared with the group taking placebo, only side effects were noted.

The substance was able to reduce Aβ levels in CSF and was associated to a greater reduction in Aβ plaques density compared to placebo. But no positive clinical effect was shown.

Even though Lanabecestat was generally well tolerated, psychiatric adverse events were numerically greater in treatment groups compared with placebo group and were consistent with dose dependence. Lanabecestat exposure was also associated with hair color changes and weight loss. 

Full text:


In two new, randomized clinical trials, Lanabecestat (a potent Aβ inhibitor) did not slow cognitive or functional decline of AD compared with placebo. One more hope of treatment has failed. It appears unlikely that current BACE inhibitors will be an effective disease modifying treatment for symptomatic AD but future studies are still needed to determine if reduction in Aβ production can provide meaningful clinical benefit in earlier stages of the disease continuum or in other high-risk populations. 

 PREVENTION is still the best solution!

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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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Despite the significant health problem posed by the disease, only five medical treatments are approved for Alzheimer’s disease (AD), which are intended to control symptoms rather than change the course of the disease. By understanding the overlapping mechanisms of AD pathology, it is possible to get an idea of the complexity of this problem. The treatments currently available have shown frustrating results and some serious side effects that can aggravate a common problem in older people: polypharmacy – many drugs are prescribed, one to cure the side effects caused by the other. While some potential future drugs are being tested, most of them targeting directly at amyloid or tau protein, it is clear that prevention is currently the safest and most effective way to combat AD.

You can find out more about this topic on this page at KsD…

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