What Is Brain Plasticity?

This is Brain Awareness Week, March 15 to 21 and there is growing evidence that suggests that promoting sleep maybe useful to restore synaptic plasticity in different pathological conditions.  Since plastic processes are essential for functional recovery, management of the sleep-wake cycle in patients and an adequate treatment of associated sleep disturbances could be crucial for the rehabilitation outcome. 

I did some reading of a few studies on how Brain Plasticity may help us. I have tried to summarize what I read below but remember these are my interpretations of some interesting articles I found by doing a google search on brain plasticity and sleep and reviewing the scientific journals that came up in the search. (The pandemic restrictions gives us lots of free time to explore.)

 Essentially, the human brain is a collection of nerve cells. These cells are communicated with by chemicals called neurotransmitters, which are released by various organs in the body in response to various stimuli. This helps to form emotions and many medications work by interacting with neurotransmitters and their receptors.

 The cells of the brain don't only communicate via neurotransmitters; they can also communicate with adjacent cells via electrical impulses. This means that the geographical layout of the brain is more important than was once realized.

 That's where brain plasticity, also called "neuroplasticity" or “Neuronal plasticity” and the science of plasticity psychology comes in and there are some suggestions that the neuronal plasticity may help in the treatment of Obstructive sleep apnea (OSA).

 OSA is a common breathing and sleep disorder, characterized by cessations or reduction in respiration due to pharyngeal collapse during sleep that induce intermittent hypoxia and sleep fragmentation increasing daytime sleepiness and risk for cardiovascular disease. OSA is associated with neurocognitive impairment, with negative influence on vigilance, attention, executive functioning, and memory.

Results from recent studies by H. Xie and W.H. Yung suggests that changes in synaptic plasticity could account for cognitive impairment in OSA patients. A better understanding of the plastic changes occurring in OSA patients, as well as their possible role in cognitive impairment, is of great importance at a therapeutic level.

 In a study done by M. M. Ohayon, M. A. Carskadon, C. Guilleminault, and M. V. Vitiello, found that sleep in patients affected by Alzheimer’s disease (AD) is characterized by a general accentuation of the sleep modifications which are observed in normal ageing. Different studies have found an EEG slowing during a condition of resting wakefulness in AD and Mild Cognitive Impairment (MCI) patients.

 Albeit the mechanisms underlying the beneficial melatonin effects in AD and MCI remain unclear, Kang and co-workers have found in mice that sleep reduces synaptic anomalies associated with amyloid precursor protein (APP), one of the typical synaptic alterations observed in AD. These data raise the possibility that the positive effects of sleep in AD and MCI are associated with an enhancement of synaptic plasticity. Since plastic processes are strongly impaired in AD patients, a reduction of sleep alterations could be useful to restore synaptic plasticity and to limit or to slow down the cognitive decline in such patients.

The prevalence of sleep disorders in children with autism ranges from 40% to 80%. Sleep in autistic children is characterized by long sleep latency, nocturnal awakenings, short sleep duration, low sleep efficiency, circadian rhythm disturbances, increased REM density and stage 1 sleep, reduction of REM sleep and SWS, and decreased spindle activity. Moreover, behavioural insomnia syndromes and REM sleep behaviour disorder have been often observed.

Different studies have found a deficit in melatonin secretion in autistic patients that seems to represent a risk factor (and not a consequence) of autism.

Recently it has been proposed that learning disabilities in autisms are related to an abnormally high LTP linked with pineal hypofunction, low serum melatonin levels, and sleep dysfunction. According to a recent study by A. J. Yun, K. A. Bazar, and P. Y. Lee, promoting sleep by means of a melatonin treatment may reduce learning disabilities by restoring the synaptic plasticity. Melatonin treatment improves sleep quality in autistic patients and secretin, a hormone that stimulates melatonin, induces a temporary improvement of autism symptoms.