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!

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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: https://jamanetwork.com/journals/jamaneurology/fullarticle/2755347


Conclusion:

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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