Current research suggests that there is a link between the lack of sleep and the subsequent development of Alzheimer. Multiple articles and studies have been published exploring this subject and I have provided some links to them below.
A study conducted in April 2018 by the National Institute of Alcohol Abuse and Alcoholism found that losing only one night of sleep leads to an increase in beta-amyloid, a protein associated with Alzheimer’s disease found in the brain. The beta-amyloid proteins coagulate forming amyloid plaques in the brain- these plaques are typical traits of Alzheimer. Beta-amyloid is a “metabolic waste product present in the fluid between brain cells”.
The formation of beta-amyloid plaques is believed to directly impair neurone communication and the plaques are considered neurotoxic.
A further study that also explores the link between sleep deprivation and Alzheimer was conducted by the Centre for Translational Neuromedicine. This study discovered that the glymphatic clearance pathway, which clears waste for the central nervous system, is ten time more active whilst we are asleep compared to when we are awake. The glymphatic system clears away beta-amyloid plaques and without sufficient sleep the system is unable to clean.
It was also found in a study at the University of Rochester Medical School that whilst mice slept, cells in the brain shrank, facilitating a greater volume of fluid to pass between the cells, aiding the removal of the buildup of neurotoxic molecules.
Furthermore, scientists at the University of Toronto found that adequate sleep led to the inhibition of the APOE-E4 gene- a gene typically associated with the development of late-onset Alzheimer. The study also showed that participants who carried the APOE-E4 gene and slept well had better retention of memories and thinking skills.
The results produced by these studies provides convincing evidence for the link between sleep deprivation and the development of Alzheimer- however further studies are needed for this relationship to be understood completely.
1. NIH/National Institute on Alcohol Abuse and Alcoholism. “Lack of sleep may be linked to risk factor for Alzheimer’s disease: Preliminary study shows increased levels of beta-amyloid.” ScienceDaily. ScienceDaily, 13 April 2018. .
2. https://www.alzheimers.net/2013-10-29/lack-of-sleep-may-cause-alzheimers/ [Accessed 30/04/2018]
3. https://www.alzinfo.org/articles/poor-sleep-may-be-linked-to-alzheimers-disease/ [Accessed 30/04/2018]
An article published on Science Daily (linked below) led me to write this post about the possibility of the alleviation of the social deficits associated with Autism Spectrum Disorder, it detailed the possibility of using an anti-cancer drug to treat the symptoms of ASD.
Current treatments of Autism Spectrum Disorder include behaviour management techniques, the administration of psychotropic drugs including selective serotonin re-uptake inhibitors (SSRIs) and anti-psychotics. Behaviour management techniques include teaching positive behaviours and reducing negative ones, this can include teaching interpersonal skills and reducing anti-social behaviours such as echolalia and inconsistent eye contact. The prescription of SSRIs is meant to treat conditions such as depression, anxiety and obsessive compulsive behaviours that are closely associated with the Disorder. Anti-psychotics are commonly used in treating the symptoms; these include treating aggression, self injury and hyperactivity.
New research conducted at the University of Buffalo suggests that the use of a single drug instead of a combination of treatments, may be efficacious in mitigating the anti-social behaviours associated with the Disorder. The research presented the possibility that the administration of low doses of romidepsin, a drug typically used to treat cutaneous and peripheral T-Cell Lymphoma, could be effective in reversing social deficits. During the research, mice lacking in the gene Shank-3, a risk factor in Autism Spectrum Disorder, were administered very low doses of romidepsin in a three-day treatment. The effects of the administration were long lasting, spanning three weeks. What should be noted is that there is currently no treatment available to treat the main symptom of ASD- the social deficits.
Shank-3 typically provides instructions for synthesising proteins that are found most commonly in the brain. The gene plays a role in the function of the synapses supporting the connections between neurons. Gene mutations within the Shank-3 gene have been identified in people with ASD. The mutations either completely inhibit the production of the gene, or disturbs the production of the proteins. It is currently not known how this mutation relates to the development of ASD however it is hypothesised that the disturbance of the connection between neurons is an influencing factor.
Romidepsin works by reconstituting the expression of genes and their functions through the use of epigenetic mechanisms. This is done by genes being changed through influences not including DNA sequencing.
This research indicates a revolutionary new field of treatment for people living with the ASD, and could lead to exciting new developments in treatment and management of the Disorder.
Original Article: https://www.sciencedaily.com/releases/2018/03/180312201647.htm [Accessed 30/04/2018]
1. https://ghr.nlm.nih.gov/gene/SHANK3 [Accessed 30/04/2018]
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2171144/ [Accessed 30/04/2018]
3. https://www.ncbi.nlm.nih.gov/pubmed/20687077 [Accessed 30/04/2018]