The edible mushroom Hericium erinaceus is increasingly becoming the focus of dementia research. Thanks to its bioactive substances such as hericenone and erinacine, the mushroom exhibits a variety of neuroprotective properties. These have already been proven in clinical studies with Alzheimer's patients, where they led to an improvement in cognitive abilities.
α -Lipoic acid is a short-chain fatty acid that can be produced by the body itself as well as absorbed through food and dietary supplements. In addition to its role as a pro-energetic and antioxidant, it has a number of other positive effects in the body and, according to numerous studies, can counteract the progression of dementia diseases such as Alzheimer's.
At regular intervals, we would like to draw your attention to current articles from the Internet that are closely related to our core topic of lifestyle-oriented and self-responsible prevention and treatment of dementia and their relevance. The opinions expressed in the above articles are intended to serve as a stimulus for critical debate. They do not necessarily correspond to the positions we represent, but in all cases they enrich the basis for discussion. At the end of each press article we refer to our scientifically based KsD articles - please take a look for yourself!
The cold shock protein RBM3, which is increasingly produced in the cold, has shown neuroprotective properties in numerous cell culture and animal experiments. A study on mice by the University of Cambridge has now confirmed that RBM3 contributes to the protection of synapses and nerve cells. These findings could be of particular interest for dementia research and other neurodegenerative diseases.
A new animal model sheds light on the dark mystery of Alzeheim disease. A molecule called MEG 3 is capable of causing human brain cells to die, making it a potential risk factor for Alzeheimer's disease.
An Australian study found that antibody drugs for Alzheimer's, such as aducanumab and lecanemab, can reduce brain volumes. Despite successful reduction of Alzheimer's-specific amyloid-beta deposits, the benefit of these drugs remains questionable. They slow cognitive decline only slightly and have severe side effects. The study also suggests that these drugs promote the cardinal structural symptom of Alzheimer's disease, brain atrophy. Thus, they increase the risk of brain tissue loss, a direct cause of cognitive decline in Alzheimer's disease.
At regular time intervals, we would like to draw your attention to current reports on the Internet that are closely related to our core topic of lifestyle-oriented and self-responsible prevention and treatment of dementia and its relevance. The opinions expressed there should stimulate a critical exchange of views. They do not necessarily reflect the positions we hold, but in all cases they enrich the basis for discussion. t the end of each press article, we refer to our scientifically based KsD articles - please make up your own mind!
Since 2022 the team of the project "Knowledge stops Dementia" started to refer on a regular base to current contributions from the world wide web which have a close relation to our core topic, the early detection of individual risk factors and thus the lifestyle-oriented and self-responsible prevention and treatment of dementia-related diseases. The opinions expressed in the following articles should serve as a stimulus for critical discussion. They do not necessarily correspond to the positions we hold, but in all cases, they enrich the basis for discussion. Occasionally, we also refer to current freely available studies at the end – please make up your own mind!
The situation is escalating: While the number of Alzheimer's patients in Germany and worldwide is increasing dramatically, a pharmacological [...]
The Amyloid theory is accepted to date as the major justification for the development of Alzheimer's disease and has guided the focus of research in this area. According to this theory, the formation of amyloid plaques, often also referred to as senile plaques, that is, abnormal deposits of the amyloid beta protein (Aβ) in the brain would be the direct cause for the symptoms of this type of dementia. This theory was born in the first description of the disease in 1907, when Alois Alzheimer found a large amount of those plaques distributed in the brain of his famous patient Auguste Deter, when examining her brain after her death. In 1984, Aβ was identified as the main component of the plaques.
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