Watch Out for False Promises About So-Called Alzheimer's Cures
Unfortunately, when faced with a serious health issue, even the most rational person can be led to believe implausible claims.
Authors: Paradise DM PMID: 31201001 [PubMed - as supplied by publisher]
Authors: Li H, Habes M, Wolk DA, Fan Y, Alzheimer's Disease Neuroimaging Initiative and the Australian Imaging Biomarkers and Lifestyle Study of Aging Abstract INTRODUCTION: It is challenging at baseline to predict when and which individuals who meet criteria for mild cognitive impairment (MCI) will ultimately progress to Alzheimer's disease (AD) dementia. METHODS: A deep learning method is developed and validated based on magnetic resonance imaging scans of 2146 subjects (803 for training and 1343 for validation) to predict MCI subjects' progression to AD dementia in a time-to-event analysis setting. RESUL...
Authors: Strandberg TE, Tienari PJ PMID: 31201097 [PubMed - as supplied by publisher]
Abstract Brief stereotaxic insertion and removal of a microneedle into the hippocampus of mice result in stimulation of hippocampal neurogenesis. This approach has been previously applied to a mouse model of Alzheimer's disease (Song et al., Cell Transplant 25:1853-1861, 2016). Further studies of fundamental cellular mechanisms of the brain's response to micro-injury will be useful for investigation of potential neuroprotective and deleterious effects of targeted microlesions and deep brain stimulation in neurodegenerative diseases. PMID: 30656634 [PubMed - indexed for MEDLINE]
In this study, analysis of antioxidant defense was performed on the blood samples from 184 "aged" individuals aged 65-90+ years, and compared to the blood samples of 37 individuals just about at the beginning of aging, aged 55-59 years. Statistically significant decreases of Zn,Cu-superoxide dismutase (SOD-1), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were observed in elderly people in comparison with the control group. Moreover, an inverse correlation between the activities of SOD-1, CAT, and GSH-Px and the age of the examined persons was found. No age-related changes in glutathione reductas...
Publication date: Available online 14 June 2019Source: Neurología (English Edition)Author(s): T. Casadevall Codina, F. Espada Olivan, C. Guerrero Castaño, N. Ruscalleda Morell
AbstractAdult neurogenesis defects have been demonstrated in the brains of Alzheimer ’s disease (AD) patients. The neurogenesis impairment is an early critical event in the course of familiar AD (FAD) associated with neuronal loss. It was suggested that neurologic dysfunction in AD may be caused by impaired functioning of hippocampal neural stem cells (NSCs). Multiple metabolic an d structural abnormalities in neural mitochondria have long been suspected to play a critical role in AD pathophysiology. We hypothesize that the cause of such abnormalities could be defective elimination of damaged mitochondria. In the pre...
Conclusion: Aβ42 and tau seem to be worthy candidates for future salivary biomarkers for AD, but other biomarkers such as lactoferrin and selected metabolites also have potential. More studies must be carried out with larger sample sizes and a standardization of the sampling and processing method. Factors such as diurnal variation, AD patients' decreased ability of oral self-care, and salivary flowrates must be taken into consideration. PMID: 31191751 [PubMed - in process]
Publication date: 15 June 2019Source: New Scientist, Volume 242, Issue 3234Author(s): Debora MacKenzieAn arthritis drug might prevent Alzheimer's, but the firm that owns it isn't keen to develop it. Debora MacKenzie reports
Authors: Rosenberg PB, Outen M S JD, Amjad M D M P H H, Burhanullah M D MH, Vandrey Ph D R, Monette B A PJ, Forester M D M Sc BP PMID: 31196620 [PubMed - as supplied by publisher]