Why freshwater hydra does not get Alzheimer’s disease

Abstract

The history of research into the basic mechanisms of the pathogenesis of Alzheimer’s disease (AD) is briefly considered. Concepts are analyzed in which a decisive role in the development of this disease was attributed to aluminum or free radicals. The lack of reliable data to date to support these concepts is emphasized. The point of view of the author is presented, according to which almost all the results indicating the feasibility of using antioxidants (as well as other potential drugs for AD) for the prevention and treatment of AD were obtained on model animals with certain pathologies (for example, with severe oxidative stress), which contribute to the formation of symptoms similar to those of AD in humans. In this regard, parallels are drawn with experimental gerontological research aimed at studying the effect of a calorie-restricted diet on aging and life span. It is noted that in these studies, animals were used that were either not completely normal or were in unfavorable conditions. According to the author, the lack of significant progress in the development of effective geroprotectors or drugs for the prevention/ treatment of AD is due to the fact that most specialists ignore the principles of classical gerontology, in particular, the definitions of aging and age-related diseases, as well as the correct approaches to the selection of control objects for their studies. It is emphasized that humans, unfortunately, cannot use the freshwater hydra method to combat aging and age-related diseases. Under certain conditions, it continuously renews all cells (including nerve ones) of its body and thereby ensures its “immortality.” In humans, the replacement of “old” neurons can lead to the loss of personality/individuality, and the “repair” of these cells today seems impossible. In this regard, the author considers it expedient to study the aging of postmitotic cells in experiments on stationary cell cultures, which can accelerate, in particular, the deciphering of the mechanisms of accumulation of beta-amyloid and senile pigments such as lipofuscin in neurons. The need for clinical studies of AD is noted as complementary to experimental work, although the first ones are much more expensive and time-consuming. Only confirmation in human studies of the effectiveness of drugs developed in experiments on model animals will allow them to be recommended for use in the clinical practice.