How insomnia can increase your risk of Alzheimer’s disease¹

Dementia is one of the major causes of disability and death in elderly people. People afflicted with dementia have difficulties with memory, language, problem-solving, and cognitive (intellectual) decline, that can affect their daily routine and social activities. Alzheimer’s disease is the most common type of dementia, accounting for 60 – 80 % of dementia cases.^1,2

Alzheimer’s disease is a progressive disease (gets worse over time), where dementia symptoms gradually worsen over several years. In its early stages, memory loss is mild, but with late-stage Alzheimer’s disease, people lose the ability to carry on a conversation and respond to their environment. Risk factors for developing Alzheimer’s disease include advancing age, genetic factors and sleep disturbances (e.g. sleep deprivation and insomnia).^1,2,3

A healthy human brain contains tens of billions of neurons. These are specialised cells that process and transmit information via electrical and chemical signals – sending messages between different parts of the brain, and from the brain to the muscles and organs in the body. Alzheimer’s disease disrupts this communication amongst neurons, resulting in loss of function and cell death.

1. Communication. Neurons are constantly in contact with nearby brain cells. When a neuron receives signals from other neurons, it generates an electrical charge that travels down the length of its axon and releases neurotransmitter chemicals across a tiny gap (synapse). Each neurotransmitter molecule then binds to specific receptor sites on a dendrite of a neighbouring neuron triggering chemical or electrical signals that either stimulate or inhibit activity in the neuron receiving the signal. Communication often occurs across networks of brain cells.⁴

2. Metabolism. The breaking down of chemicals and nutrients within a cell is critical to healthy cell function and survival. To perform this function, cells require energy in the form of oxygen and glucose, which are supplied by blood circulating through the brain.⁴

3. Repair, remodelling, and regeneration. Many of the cells in the body have a relatively short life. Neurons, on the other hand, have evolved to live a long time (more than 100 years in humans). Accordingly, they need to constantly maintain and repair themselves. Neurons also continuously adjust (remodel) their synaptic connections depending on how much stimulation they receive from other neurons e.g. they may strengthen or weaken synaptic connections, or even break down connections with one group of neurons and build new connections with a different group. Adult brains may even generate new neurons—a process called neurogenesis. Remodelling of synaptic connections and neurogenesis are important for learning, memory, and possibly brain repair.⁴

Other cells in the brain, called glial cells, surround and support the function and health of neurons. Microglia, a type of glial cell, protect neurons from physical and chemical damage and are responsible, with the aid of blood vessels, for clearing cellular debris and foreign substances from the brain.⁴

With healthy aging, the brain will shrink to some degree, but does not lose large numbers of neurons. In Alzheimer’s disease, many neurons stop functioning, lose connections with other neurons, and die. Alzheimer’s disease disrupts the processes, described above, that are vital to neurons and their networks.⁴

Amyloid plaques. Abnormal levels of a naturally occurring protein, beta-amyloid, clump together to form deposits (plaques) between neurons and disrupt cell function.^2,4

Neurofibrillary tangles. Abnormal chemical changes cause another protein, called tau, to stick to other tau molecules, forming threads that eventually join to form tangles inside neurons. These tangles block the neuron’s transport system, which harms the synaptic communication between neurons.⁴

Long-term (chronic) inflammation. This may be caused by the build-up of glial cells (microglia), meaning that waste, debris, toxins, and beta-amyloid plaques are not cleared away.⁴

Blood vessel problems. This may lead to reduced blood flow and oxygen to the brain, as well as the breakdown of the blood-brain barrier – preventing glucose from reaching the brain and preventing the clearing away of toxic beta-amyloid and tau proteins.⁴

Loss of neuronal connections and cell death. As neurons are injured and die throughout the brain (in a person suffering from Alzheimer’s disease), connections between networks of neurons may break down, causing regions of the brain to start shrinking. By the final stages of Alzheimer’s, this process is widespread and causes significant loss of brain volume.⁴

Alzheimer's changes typically begin in the part of the brain that affects learning. As Alzheimer's disease advances through the brain, it leads to increasingly severe symptoms, including disorientation, mood and behaviour changes; deepening confusion about events, time and place; unfounded suspicions about family, friends and professional caregivers; more serious memory loss and behaviour changes; and difficulty speaking, swallowing and walking.²

Sleep deprivation and insomnia can trigger the accumulation of beta-amyloid and tau proteins, inflammation, disruption to the blood-brain barrier and decline in other proteins (called neurotrophins) that are essential for survival and functioning of neurons. All these changes, as described above, can increase your risk of developing Alzheimer’s disease.¹

You can reduce your risk of developing dementia by getting adequate sleep. Researchers have found that better sleep can promote the clearing away of beta-amyloid and other substances that accumulate in the brain during the day and reduce the risk of tau protein tangles (in people who were at increased genetic risk of developing Alzheimer’s disease).

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In preparing this article, every effort has been made to provide an objective overview. The content contained in this article contains medical or health sciences information as per cited articles for public information. The content of this article has been initiated and is brought to you by Sanofi South Africa.