The new Alzheimer’s drug Lecanemab: miracle drug or flop? Take a look for yourself!
The situation is escalating: While the number of Alzheimer's patients in Germany and worldwide is increasing dramatically, a pharmacological [...]
Breaking News: Possible fraud in Alzheimer’s research puts the “Amyloid-plaque theory” into question!
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.
New trails on anti-Amyloid drug failed
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.
Statins and Dementia: Better keep your brain cells alive!
Several million patients in Germany are treated with statins. In 2004, the consumption of lipid-lowering drugs throughout Germany amounted to around 856 million defined daily doses (DDD). In 2011 the amount increased to: 1.718 million DDD. With the target to lower cholesterol levels, this doubtful strategy is still being mistakenly promoted to reduce heart disease risk. As a side effect, doctors and patients are accepting a possible cognitive decline. These are the results of a study published in 2018 in the journal Frontiers in Neurology, which looked into the relationship between cholesterol and cognitive function [1]. While cholesterol is still largely vilified, and statin use still heavily promoted, the study found that having lower levels of low-density lipoprotein (LDL) cholesterol is linked to a higher risk of dementia.
