Introduction: Currently available drugs against Alzheimer’s disease (AD) target cholinergic and glutamatergic neurotransmissions without affecting the underlying disease process. Putative disease-modifying drugs are in development and target β-amyloid (Aβ) peptide and tau protein, the principal neurophatological hallmarks of the disease. Areas covered: Phase III clinical studies of emerging anti-Aβ drugs for the treatment of AD were searched in US and EU clinical trial registries and in the medical literature until May 2016. Expert opinion: Drugs in Phase III clinical development for AD include one inhibitor of the β-secretase cleaving enzyme (BACE) (verubecestat), three anti-Aβ monoclonal antibodies (solanezumab, gantenerumab, and aducanumab), an inhibitor of receptor for advanced glycation end products (RAGE) (azeliragon) and the combination of cromolyn sodium and ibuprofen (ALZT-OP1). These drugs are mainly being tested in subjects during early phases of AD or in subjects at preclinical stage of familial AD or even in asymptomatic subjects at high risk of developing AD. The hope is to intervene in the disease process when it is not too late. However, previous clinical failures with anti-Aβ drugs and the lack of fully understanding of the pathophysiological role of Aβ in the development of AD, put the new drugs at substantial risk of failure.

Panza, F., Seripa, D., Solfrizzi, V., Imbimbo, B. P., Lozupone, M., Leo, A., Sardone, R., Gagliardi, G., Lofano, L., Creanza, B. C., Bisceglia, P., Daniele, A., Bellomo, A., Greco, A., Logroscino, G., Emerging drugs to reduce abnormal β-amyloid protein in Alzheimer’s disease patients, <<EXPERT OPINION ON EMERGING DRUGS>>, 2016; 21 (4): 377-391. [doi:10.1080/14728214.2016.1241232] [http://hdl.handle.net/10807/95360]

Emerging drugs to reduce abnormal β-amyloid protein in Alzheimer’s disease patients

Creanza, Bianca Claudia;Daniele, Antonio;
2016

Abstract

Introduction: Currently available drugs against Alzheimer’s disease (AD) target cholinergic and glutamatergic neurotransmissions without affecting the underlying disease process. Putative disease-modifying drugs are in development and target β-amyloid (Aβ) peptide and tau protein, the principal neurophatological hallmarks of the disease. Areas covered: Phase III clinical studies of emerging anti-Aβ drugs for the treatment of AD were searched in US and EU clinical trial registries and in the medical literature until May 2016. Expert opinion: Drugs in Phase III clinical development for AD include one inhibitor of the β-secretase cleaving enzyme (BACE) (verubecestat), three anti-Aβ monoclonal antibodies (solanezumab, gantenerumab, and aducanumab), an inhibitor of receptor for advanced glycation end products (RAGE) (azeliragon) and the combination of cromolyn sodium and ibuprofen (ALZT-OP1). These drugs are mainly being tested in subjects during early phases of AD or in subjects at preclinical stage of familial AD or even in asymptomatic subjects at high risk of developing AD. The hope is to intervene in the disease process when it is not too late. However, previous clinical failures with anti-Aβ drugs and the lack of fully understanding of the pathophysiological role of Aβ in the development of AD, put the new drugs at substantial risk of failure.
2016
Inglese
Panza, F., Seripa, D., Solfrizzi, V., Imbimbo, B. P., Lozupone, M., Leo, A., Sardone, R., Gagliardi, G., Lofano, L., Creanza, B. C., Bisceglia, P., Daniele, A., Bellomo, A., Greco, A., Logroscino, G., Emerging drugs to reduce abnormal β-amyloid protein in Alzheimer’s disease patients, <<EXPERT OPINION ON EMERGING DRUGS>>, 2016; 21 (4): 377-391. [doi:10.1080/14728214.2016.1241232] [http://hdl.handle.net/10807/95360]
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10807/95360
Citazioni
  • ???jsp.display-item.citation.pmc??? 19
  • Scopus 54
  • ???jsp.display-item.citation.isi??? 52
social impact