title: Rethinking Alzheimer's disease therapy: are mitochondria the key?
abstract: The number of people suffering from Alzheimer's disease (AD) is constantly increasing worldwide since humans live longer and age is the strongest risk factor for AD. Currently available medications for AD do not interfere with the progressive loss of synapses and neurons in the AD brain. Therefore, the development of disease modifying therapies is a major future goal. Mitochondria provide cellular energy and are crucial for proper neuronal activity and survival. Mitochondrial dysfunction is evident in early stages of AD and is involved in AD pathogenesis. The development of drugs that protect mitochondria from damage is therefore a promising strategy for AD therapy. In this review, we will discuss current available medications for AD, drugs under clinical testing, and mitochondria as a novel drug target.
authors.affiliation: KI-Alzheimer's Disease Research Center, Karolinska Institutet, Department of Neurobiology, Care Sciences and Society (NVS), Huddinge, Sweden. maria.ankarcrona@ki.se
authors.forename: Maria
authors.initials: M
authors.lastname: Ankarcrona
authors.forename: Francesca
authors.initials: F
authors.lastname: Mangialasche
authors.forename: Bengt
authors.initials: B
authors.lastname: Winblad
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy* / Q000473:pathology*; D000818:Animals; D014150:Antipsychotic Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D006801:Humans; D008928:Mitochondria / Q000187:drug effects* / Q000502:physiology*
chemical_list: D014150:Antipsychotic Agents