As one ages, being diagnosed with dementia becomes increasingly likely. As recorded by the Alzheimer’s Association, out of the approximately 5.5 million Americans in 2017 who were diagnosed with dementia, around 5.3 million are 65 and older. As such, different communities are investigating different ways to facilitate those suffering from the disease, and their caretakers.
In Singapore (where two years ago a study found that 10% of people aged 60 and over suffered from dementia) a community-wide Dementia Prevention Programme (DPP) was piloted a year ago in Queenstown and Eunos. Since then, reports have shown that there has been an enhancement in quality of life for seniors vis-à-vis “social connectedness and life satisfaction.” According to the National University Health System (one of the supporters of the project) participants reported a reduction in both anxiety and depression after three months. Five activities were included in the study: exercise, health education, horticulture therapy, “meridian flapping” (a simple and effective technique to improve body Qi-Energy flow), mindfulness awareness practice and music reminiscence.
Meanwhile there is some good news for dementia sufferers. A few years ago, a UK-based team of Medical Research Council (MRC) scientists identified a key route to the dissolution of brain function in mice. As such they went on to discover two blocking drugs which can inhibit neurodegeneration.
The understanding was that there is an expansion in the brain of misfolded proteins that were seen in various several neurodegenerative diseases, which are a key factor in conditions like Alzheimer’s and Parkinson’s and other prion diseases. The most recent finding was that switching protein production back on with an experimental drug, was able to freeze neurodegeneration that results in these diseases. Unfortunately though, the drug tested was toxic to the pancreas and not suitable for testing in humans.
Last month a study was undertaken in which 1040 compounds from the National Institute for Neurological Disorders and Stroke were tested initially in worms (C.elegans) that have a functioning nervous system and are a good experimental model for screening drugs to be used on the nervous system and then in mammalian cells. Some suitable candidate compounds were found that could then be tested in mouse models of prion disease and a form of familial tauopathy (frontotemporal dementia – FTD), both of which had been protected by the experimental – but toxic – compounds in the team’s previous studies. At that point two drugs that were able to restore protein production rates in mice (trazodone hydrochloride, a licensed antidepressant, and dibenzoylmethane (DBM), a compound being trialled as an anti-cancer drug) were identified. Both were able to prevent the appearance of brain cell damage indication in most of the mice with prion condition, restoring memory in the FTD mice. Drugs were then able to reduce brain contraction – part of neurodegenerative diseases.
Study team leader Professor Giovanna Mallucci further explained:
“We know that trazodone is safe to use in humans, so a clinical trial is now possible to test whether the protective effects of the drug we see on brain cells in mice with neurodegeneration also applies to people in the early stages of Alzheimer’s disease and other dementias. We could know in 2-3 years whether this approach can slow down disease progression, which would be a very exciting first step in treating these disorders. Interestingly, Trazodone has been used to treat the symptoms of patients in later stages of dementia, so we know it is safe for this group. We now need to find out whether giving the drug to patients at an early stage could help arrest or slow down the disease through its effects on this pathway.”
