NIH PubMed latest 20 review articles on Alzheimer's

Second-generation antipsychotics in dementia: beyond safety concerns. A clinical, systematic review of efficacy data from randomised controlled trials.

Gentile S

Second-generation antipsychotics in dementia: beyond safety concerns. A clinical, systematic review of efficacy data from randomised controlled trials.

Psychopharmacology (Berl). 2010 Jul 27;

Authors: Gentile S

RATIONALE: Antipsychotic drugs are widely used as a first-line pharmacological approach to treat dementia-related psychiatric symptoms. However, in this population of patients, such drugs have been associated with severe safety concerns. Hence, the aim of this review is to asses systematically the efficacy of second-generation antipsychotics (SGAs) in treating dementia-related neuropsychiatric symptoms in order to establish if the potential clinical benefits of such treatment outweigh the hypothesised risks related to pharmacological intervention. METHODS: The Cochrane Library, MEDLINE, EMBASE and PsycINFO were searched (from 1980 to June 22, 2010) using terms for included drugs (aripiprazole, clozapine, olanzapine, quetiapine, risperidone, ziprasidone, SGAs) and indications (elderly, dementia, Alzheimer's disease). Electronic database search were supplemented with hand search of references lists of electronically identified articles. Peer-reviewed, randomised, controlled trials published in English and investigating the efficacy of SGAs in patients with different forms of dementia were included in the review process. Information was drawn from the 30 articles that met the inclusion criteria. RESULTS: Nearly all reviewed studies suffer from methodological limitations too severe to draw definitive conclusions that may inform the decision-making process. Moreover, studies conducted with similar methodological design show conflicting efficacy results. CONCLUSIONS: Because of their undemonstrated effectiveness, SGAs should be avoided in patients with dementia complicated by psychotic and/or behavioural symptoms. Hence, further researches are urgently needed to identify useful pharmacological strategies that can be used to improve the clinical condition of such patients and to reduce burden to caregivers when behavioural interventions are ineffective.

PMID: 20661553 [PubMed - as supplied by publisher]

Lithium-mediated protection against ethanol neurotoxicity.

Luo J

Lithium-mediated protection against ethanol neurotoxicity.

Front Neurosci. 2010;4:41

Authors: Luo J

Lithium has long been used as a mood stabilizer in the treatment of manic-depressive (bipolar) disorder. Recent studies suggest that lithium has neuroprotective properties and may be useful in the treatment of acute brain injuries such as ischemia and chronic neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis. One of the most important neuroprotective properties of lithium is its anti-apoptotic action. Ethanol is a neuroteratogen and fetal alcohol spectrum disorders (FASD) are caused by maternal ethanol exposure during pregnancy. FASD is the leading cause of mental retardation. Ethanol exposure causes neuroapoptosis in the developing brain. Ethanol-induced loss of neurons in the central nervous system underlies many of the behavioral deficits observed in FASD. Excessive alcohol consumption is also associated with Wernicke-Korsakoff syndrome and neurodegeneration in the adult brain. Recent in vivo and in vitro studies indicate that lithium is able to ameliorate ethanol-induced neuroapoptosis. Lithium is an inhibitor of glycogen synthase kinase 3 (GSK3) which has recently been identified as a mediator of ethanol neurotoxicity. Lithium's neuroprotection may be mediated by its inhibition of GSK3. In addition, lithium also affects many other signaling proteins and pathways that regulate neuronal survival and differentiation. This review discusses the recent evidence of lithium-mediated protection against ethanol neurotoxicity and potential underlying mechanisms.

PMID: 20661453 [PubMed - in process]

Inhibition of BACE1 for therapeutic usein Alzheimer's disease.

Luo X, Yan R

Inhibition of BACE1 for therapeutic usein Alzheimer's disease.

Int J Clin Exp Pathol. 2010;3(6):618-28

Authors: Luo X, Yan R

Since BACE1 was reported as the beta-secretase in Alzheimer's disease (AD) over ten years ago, encouraging progress has been made toward understanding the cellular functions of BACE1. Genetic studies have further confirmed that BACE1 is essential for processing amyloid precursor protein (APP) at the beta-secretase site. Only after this cleavage can the membrane-bound APP C-terminal fragment be subsequently cleaved by gamma-secretase to release so-called AD-causing Abeta peptides. Hence, in the past decade, a wide variety of BACE1 inhibitors have been developed for AD therapy. This review will summarize the major historical events during the evolution of BACE1 inhibitors designed through different strategies of drug discovery. Although BACE1 inhibitors are expected to be safe in general, careful titration of drug dosage to avoid undesirable side effects in BACE1-directed AD therapy is also emphasized.

PMID: 20661410 [PubMed - in process]

[Advances in anti-beta antibody treatment of Alzheimer's disease]

Zhang JH, Liang P

[Advances in anti-beta antibody treatment of Alzheimer's disease]

Zhonghua Bing Li Xue Za Zhi. 2007 Sep;36(9):633-5

Authors: Zhang JH, Liang P

PMID: 18070457 [PubMed - indexed for MEDLINE]