Slowing the progression of Alzheimer’s disease

For Alzheimer's Awareness Day, we discuss the latest recommended articles covering potential tools and techniques for early diagnosis of Alzheimer's disease and to help improve our cognitive function.

Alzheimer's disease

Image credit: Susan Lockhart, Wellcome Images, CC BY-NC 4.0

‘AI can identify Alzheimer’s disease a decade before symptoms occur’, claimed a recent headline, announcing that a machine-learning algorithm can identify structural changes in the brain caused by Alzheimer’s disease. This is just one of many research attempts to diagnose the disease as early as possible. Early detection of the diseases means it can be managed in a better way and improve research into new potential treatments.

Alzheimer’s disease is the most common form of dementia. In 2013, there were 44.4 million people with the disease. By 2050, this is predicted to rise to 135.5 million. A study in 2014 found that 99.6% of clinical trials for Alzheimer’s disease failed. These startling figures underlie the urgent need to find a cure.

While there is, as of yet, no cure for Alzheimer’s disease, there are interventions and drugs that can help slow the progression of the disease or treat the symptoms. While the search for a cure continues so does research into how to identity the disease and slow down the decline of people with the condition. For Alzheimer’s Awareness Day, we share a few of the latest recommended articles of the potential tools and techniques that can help improve our cognitive function and aid with early detection.

 

Chunking

Our working memory has a limited capacity. It can only focus on a few items of information, meaning that us humans must use strategies to mentally retain information. One such strategy is ‘chunking’, a process whereby we compress information into a more manageable state. We do this by recognising patterns within the information and applying them to simplify it to create ‘chunks’ of information that can be held within the limited capacity of our working memory.

Research published in The British Journal of Psychiatry, and recommended in F1000Prime, explains that this ability is preserved in the early stages of Alzheimer’s disease, and is being used as a cognitive training method, to improve the brain’s working memory.

The analysis involved 30 patients with mild Alzheimer’s who had 18 sessions of 30 minutes of either adaptive chunking training or an active control intervention. ‘Chunking’ significantly improved the verbal working memory, as well as general cognition. Faculty Members, Craig Ritchie, University of Edinburgh, UK, and Abel Koshy, Dorset Healthcare University NHS Trust, UK, recommended the article and summarised: “Chunking-based cognitive training is therefore a simple and potentially achievable intervention to improve cognitive function in early AD.”

Image credit: Stephen Magrath, Wellcome Images

 

Tau tangles

From novel cognitive training paradigms to improve cognitive function in Alzheimer’s patients, researchers are also studying molecular mechanisms to understand the biological triggers of the disease.

There are no mechanism-based therapies to treat Alzheimer’s, so a study published in Nature looked at tau filaments. Neurofibrillary lesions in the cerebral cortex are a strong indicator of a cognitive deficit, such as Alzheimer’s disease, and these lesions consist of paired helical and straight tau filaments. Using brain samples from a 74 year old female patient, the researchers analysed these distinct filament morphologies and their different structures.

Faculty Member, Berl Oakley, University of Kansas, US, said “This paper reports the first structure of tau filaments from an Alzheimer’s patient. Understanding the structure of tau filaments will undoubtedly be of great value in understanding and combating this increasingly prevalent, tragic, and expensive disease.”

Image credit: Florence Winterflood, Wellcome Images, CC BY 4.0

 

A good night’s sleep

Alzheimer’s disease is also associated with neuronal changes caused by disrupted sleep, because chronic sleep deprivation can increase amyloid-β. New finding reported in Brain specifies that amyloid-β levels only increase when slow wave sleep is disrupted.

Faculty Member, Peter Brown, John Radcliffe Hospital, UK, explains: “Slow wave activity was selectively disrupted by auditory tones triggered off scalp brain wave recordings, and soluble amyloid-β measured in the cerebrospinal fluid the following morning. Slow wave sleep disruption correlated with increased amyloid-β40.” Further research is necessary to see whether these changes can be reversed, and promoting slow wave sleep activity could modify effects in patients with, or at risk of Alzheimer’s disease.

There may be no cure for Alzheimer’s, yet, but as these recommendations show, with each discovery we become better navigators gradually winding our way through and mapping out the complexities of the human brain.

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