Maria Paula Maziero, Natalia P Rocha, Antonio L Teixeira
{"title":"Antipsychotics in Alzheimer's Disease: Current Status and Therapeutic Alternatives.","authors":"Maria Paula Maziero, Natalia P Rocha, Antonio L Teixeira","doi":"10.2174/0115672050287534240215052417","DOIUrl":"10.2174/0115672050287534240215052417","url":null,"abstract":"<p><p>Psychosis and hyperactive behaviors, such as agitation and wandering, affect a significant proportion of patients with Alzheimer's disease (AD). These symptoms are often treated with antipsychotics, usually in an off-label approach. This mini-review provides an updated perspective on the pharmacological approach for the neuropsychiatric symptoms (NPS) in AD. The results of new studies have provided a better understanding of AD-related NPS management, but high-quality evidence still needs to be obtained. Herein, we argue for a more cautious approach to the use of antipsychotics in AD and highlight the importance of exploring alternative treatments for NPS. By doing so, we can ensure that patients with AD receive optimal care that is both effective and safe.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":"682-691"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139975344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Michelle C Bell, Shelby E Meier, Alexandria L Ingram, Jose F Abisambra
{"title":"PERK-opathies: An Endoplasmic Reticulum Stress Mechanism Underlying Neurodegeneration.","authors":"Michelle C Bell, Shelby E Meier, Alexandria L Ingram, Jose F Abisambra","doi":"10.2174/1567205013666151218145431","DOIUrl":"https://doi.org/10.2174/1567205013666151218145431","url":null,"abstract":"<p><p>The unfolded protein response (UPR) plays a vital role in maintaining cell homeostasis as a consequence of endoplasmic reticulum (ER) stress. However, prolonged UPR activity leads to cell death. This time-dependent dual functionality of the UPR represents the adaptive and cytotoxic pathways that result from ER stress. Chronic UPR activation in systemic and neurodegenerative diseases has been identified as an early sign of cellular dyshomeostasis. The Protein Kinase R-like ER Kinase (PERK) pathway is one of three major branches in the UPR, and it is the only one to modulate protein synthesis as an adaptive response. The specific identification of prolonged PERK activity has been correlated with the progression of disorders such as diabetes, Alzheimer's disease, and cancer, suggesting that PERK plays a role in the pathology of these disorders. For the first time, the term \"PERK-opathies\" is used to group these diseases in which PERK mediates detriment to the cell culminating in chronic disorders. This article reviews the literature documenting links between systemic disorders with the UPR, but with a specific emphasis on the PERK pathway. Then, articles reporting links between the UPR, and more specifically PERK, and neurodegenerative disorders are presented. Finally, a therapeutic perspective is discussed, where PERK interventions could be potential remedies for cellular dysfunction in chronic neurodegenerative disorders. </p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":"13 2","pages":"150-63"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6542591/pdf/nihms-1025111.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41224631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}