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!

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. 

Conclusion: 

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.  

References:

  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
Read More

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.

Conclusion:

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
Read More

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.

Conclusion: 

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

References:

  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

 

Read More

The negative effects of trans fats (also known as trans fatty acids, TFA) on our cardiovascular health have been known for a long time, they are among the most unhealthy food components of all.

In recent years, there has been an increase in the number of studies that prove an association between trans fat and  AD, as already reported by AMM in 2015 (https://spitzen-praevention.com/2015/08/14/transfettsaeuren-und-kognitive-schwaechen-da-fehlen-einem-die-worte/). 1,628 healthy Japanese seniors were followed by a current study from Japan over a period of 10 years. In this context, the researchers examined TFA elaidic acid in the blood as a marker substance, which allows direct conclusions about the total TFA intake. 377 participants developed dementia, of which 247 developed Alzheimer’s and 102 vascular dementia.  Higher serum elaidic acid levels were significantly associated with a greater risk of developing Alzheimer’s disease, vascular dementia and total dementia. Patients whose blood trans fatty acid levels were in the higher range were 90% more likely to develop Alzheimer’s disease. These relationships remained significant even after adjustment for nutritional factors, including total energy intake and the intake of saturated and polyunsaturated fatty acids.

Current situation in Germany

In the Japanese study, the TFA was consumed with sweet baked goods, crackers, ice cream and such, but what is the current exposure situation in Germany?

TFA can get into food in different ways:

  •  produced by bacterias in the rumen of ruminants (such as cows, sheep and goats) and thus enter muscle meat and milk. A health-promoting effect is even being discussed concerning these ruminant TFA.
  • industrially produced when processing vegetable oils, the so-called partial hydrogenating process. These TFA have been used extensively in industrial food production.
  • while frying and deep-frying processes, whereby the TSF are almost completely transferred from the fat into the fried food.

In 2016, the EU Commission published a draft law to limit trans fats in foods, according to which the content of industrial TSAs is to be limited to 2% in the total fat from 2021. National regulations exist only in individual member states (e.g. Denmark, Finland) and in Switzerland. The WHO has also launched a global initiative with the ‘REPLACE’ programme, which aims to eliminate it (to 1% of total calories) worldwide by 2023.

The good news is that although there is still no mandatory national regulation in Germany, fortunately, industrial TFA are virtually no longer used in pre-packaged foods. They have been almost completely replaced by palm oil or palm kernel oil, which is at least better for health, but unfortunately causes different kinds of problems. Problems with regard to TFA contents of more than 2% in total fat are posed by unpackaged, bulk or industrially-like prepared foods sold in snack bars and bakery chains, as no list of ingredients is required by law, and single cases with extremely high TFA contents are still being identified.

Risk of TFA formation by radicals in the body

Biological membranes, which occur in every cell of the body, consist of a double layer of phospholipids. They contain a high proportion of fatty acids, whereby their content of unsaturated (non-trans) fatty acids positively influences the properties of these cell membranes. Therefore, the formation of TFA in the membranes poses an apparently great danger: As soon as the fatty acids within the membranes are converted to the trans configuration and thus, TFA are generated, this can have a negative effect on the fluidity of the membrane and promote the development of chronic diseases.

A few years ago, a study showed that rats fed TFA-free food for lifetime had implemented trans-isomers of mono- and polyunsaturated fatty acids (oleic, linoleic, linolenic and arachidonic acid) in liver, kidneys, heart, adipose tissue and erythrocytes. Thus, it was proven that TFAs can be formed in the organism even if the food does not contain any TFAs. Subsequent studies have also shown that free radicals are responsible for the formation of TFAs in the body. Free radicals can be produced in the organism during essential metabolic processes under physiological conditions, but also by external influences such as cigarette smoke, air pollution, organic solvents or irradiation. Due to their high chemical reactivity, these free radicals can cause oxidative damage to cellular macromolecules. In addition, the increased occurrence of TFAs formed in the body, especially of trans arachidonic acid, has been observed due to accumulated radical stress in various pathological states, such as inflammation, diabetes and Alzheimer’s disease.

This became very obvious when a study using an Alzheimer’s animal model revealed that TFAs were found only in the brain and hippocampus of mice carrying a gene specific for Alzheimer’s disease, but not in healthy animals. This result suggests that stress due to amyloid β-mediated radicals that accumulated during the development of Alzheimer’s disease causes cis-trans isomerisation of fatty acids in neurons of Alzheimer’s mice. In a subsequent study, it was further shown that the animals had significantly reduced levels of TFA in the brain and hippocampus after administration of two antioxidant substances for 3 months. These studies thus imply that the administration of antioxidant substances may be a possible strategy to prevent the body’s own formation of TFA during the development of chronic diseases such as Alzheimer’s disease. Based on the results of all intervention studies, a variety of antioxidant vitamins and polyphenolic compounds derived from plants, including curcumin and resveratrol, appear to inhibit TFA formation in the body (Figure 1, modified after Hung et al. 2016).

Inhibition Trans Fatty Acids
Figure 1: Potential Inhibition of the Formation of Trans Fatty Acids in Human Membranes by Dietary Antioxidants

Conclusion:
The connection between Alzheimer’s disease and the consumption of trans-fatty acids (TFA) is becoming increasingly evident, although the exposure to TFA through pre-packaged food to TFA in Germany has decreased in recent years. The industry has reacted to the EU’s legal regulation, which will come into force in 2021, of a maximum of 2% of total fat. However, when you visit the snack bar and the bakery chain, remember that trans fats may still play a not inconsiderable role here.

However, the real danger of TFA seems to be in the body, as they can be produced there by free radicals. But you can do something about it with a healthy diet: Ensure your supply of antioxidant micronutrients from food and, if necessary, supplements, before the TFA otherwise formed in your body damage your cell membranes and drive you insane!

References:

  1. Honda,T et al (2019) Serum elaidic acid concentration and risk of dementia: The Hisayama Study. Neurology, 2019
  2. Informationsblatt der Europäischen Union 2019
  3. Bähr M, Jahreis G, Kuhnt K (2011) Trans fatty acids in foods on the German market and in human tissue. Ernährungsumschau 9
  4. Ghebreyesus T, Frieden TR (2018) REPLACE: a roadmap to make the world trans fat free by 2023. The Lancet 391
  5. Messdaten zu Trans-Fettsäuren aus der amtlichen Überwachung zu insgesamt 2.633 Proben aus den Jahren 2014-2017, Auskunft des Bundesamts für Verbraucherschutz und Lebensmittelsicherheit (BVL) vom 31. März 2017
  6. Kuhnt K, Degen C, Jahreis G (2015) Evaluation of the Impact of Ruminant trans Fatty Acids on Human Health: Important Aspects to Consider. Crit Rev Food Sci Nutr. 56
  7. Hung, WL et al (2016) Endogenous formation of trans fatty acids: Health implications and potential dietary intervention, Journal of Functional Foods 25

Photo by Khairul Onggon on Pexels

Read More

Red wine drinkers are generally good-natured people and known for mastering life with pleasure and relaxation. These alone are two protective factors against dementia, because stress is poison for the brain (but more about this later on). In addition, a secondary plant substance present particularly in red wine is increasingly attracting the interest of research and prevention in Alzheimer’s disease: resveratrol.

Resveratrol has numerous biological and pharmacological protective effects and became well-known back in the mid-1990s in connection with the ‘French Paradox’. It stands for the observation that French people live longer than Germans and Americans despite their supposedly unhealthier lifestyle, especially because of their higher alcohol consumption, and that the frequency of heart attacks in France is three times lower than in the USA. In the following years, resveratrol became the focus of research and showed anti-inflammatory, antioxidant, cancer-inhibiting, heart protecting and life-prolonging properties in numerous test models both in vitro and in vivo and was considered a new miracle cure.

Resveratrol and Alzheimer

The first indications that resveratrol could also be responsible for the protective effect of red wine in Alzheimer patients were shown by epidemiological studies conducted by a French research group in 1997, which showed an inverse correlation between moderate wine consumption and the occurrence of Alzheimer’s disease: in the group of moderate wine drinkers (250 – 500 ml per day) the risk of dementia was reduced by a factor of 5.

It showed that resveratrol not only unfolds its positive effects in a single way, but also has a multi-mechanistic effect. It has a beneficial effect on various processes, all of which play a decisive role in the development of Alzheimer’s disease:

  1. reduction of amyloid plaques 
  2. reduction of neurofibrillary tangles 
  3. regulatory role in autophagy processes 
  4. anti-inflammatory effect 
  5. antioxidant effects

Detailed explanations on these topics can be found on the page: Resveratrol

Clinical studies

Based on these convincing results, the therapeutic potential of resveratrol in Alzheimer’s patients is currently being tested in clinical trials. Two recent pilot studies have shown that resveratrol can easily cross the blood-brain barrier in humans and penetrate brain tissue – as it has been detected in cerebrospinal fluid. Resveratrol was well tolerated by all volunteers and had no side effects up to a dose of 5 grams per day. Both double-blind studies show evidence of positive effects of resveratrol in humans. 

In addition, resveratrol is already part of the multifactorial approach of the American neurologist Dale Bredesen, who, with his therapy known as ‘ReCode’ (Reversal of Cognitive Decline), has managed to clinically reverse Alzheimer’s courses in early stages (see also the interview with Dr. Bredesen in the media library).

Conclusion:
Whether fed with a glass of red wine in the evening or by other non-alcoholic means – but preferably from natural sources – the secondary plant substance resveratrol appears to be responsible for protective effects in the development of dementia due to its diverse mechanisms of action. It could therefore be a promising preventive and possibly therapeutic approach in the fight against Alzheimer’s disease.

In this sense: treat yourself to a glass of red wine or grape juice in the evening and enjoy life. Your grey cells will be grateful!

Read More
SPENDEN

Support us now!