For this reason, studies aimed at researching new pharmacological treatments against Alzheimer's disease focus precisely on molecules that are able, in one way or another, to prevent / eliminate the accumulations of the aforementioned proteins.
bapineuzumab and solanezumab which, however, did not produce the desired results as the studies progressed. It should be noted, however, that these molecules have been tested on individuals with advanced disease, therefore, the goal of the researchers seems to be to use the same molecules, but on patients who are in the early stages of the disease and with a mild cognitive impairment.
In the field of anti-beta-amyloid drugs there is also an active ingredient that is raising new hope and for which the results obtained seem really encouraging: it is the monoclonal antibody aducanumab. Studies - conducted on patients with Alzheimer's disease and mild cognitive decline - have shown that aducanumab is capable of reducing β-amyloid levels in brain tissues and that it is able to slow down both cognitive and functional.
However, those mentioned are just some of the anti-amyloid beta drugs that research has focused on over the years; among the other active ingredients studied are gantenerumab and crenezumabm, but also sodium oligo-mannurarate (a compound of marine origin that in a study conducted in China gave encouraging results in the treatment of patients with mild to Alzheimer's disease moderate).
However, it should be noted that the search for anti-amyloid drugs - although it is continuing - has significantly reduced over the last few years.
nervous. APP degradation can follow two different paths:
- The amyloidogenic pathway which involves the intervention of beta-secretase which splits the APP protein into two fragments: an N-terminal and a C-terminal transmembrane. The latter is then degraded by the gamma-secretase (or γ-secretase) enzyme resulting in the formation of the beta-amyloid protein.
- The non-amyloidogenic pathway which, on the other hand, involves the intervention of the enzyme alpha-secretase (or α-secretase). The latter degrades the APP protein leading to the formation of a soluble N-terminal fragment and a transmembrane C-terminal fragment. The latter will in turn be degraded by gamma-secretase into two further fragments which, however, in this case they are not toxic.
In light of what has just been said about the formation of beta-amyloid protein, it will not be surprising to know that beta-secretase is also one of the possible targets of drug therapy against Alzheimer's disease. Among the active ingredients capable of exerting an inhibitory action against the enzyme in question and to date still under study for the evaluation of efficacy and safety, we recall the "elenbecestat".
of Alzheimer's patients. Unfortunately, the studies conducted so far have not led to the desired results, but the research is still working on this front. Some of the studies currently underway are still in the early stages of clinical trials.
PLEASE NOTE
The above are just some of the possible targets and studies that aim to identify potential new drugs for the treatment of Alzheimer's disease. In this field, in fact, research has been and continues to be very extensive.
