What is it?
Alzheimer’s is the most common cause for dementia. In 95% of cases, the disease onsets when people are older than 65. Alzheimer’s affects 6% of people older than 65 and, after that, the proportion doubles every five years.
Alzheimer’s is a progressive neurodegenerative illness. This means that it gets worse over time, and it cannot be stopped or reversed. It involves the death of neurons (brain cells) in the cerebral cortex (the outer layer of the brain, which is responsible for many of the actions that we define essential to the formation of personality, such as memory, consciousness, and language).
Early symptoms can include problems with memory (such as forgetting about recent events or the names of things), anxiety, and confusion.
Middle-stage symptoms can include increasing confusion and disorientation, delusions (believing untrue things) and hallucinations (sensing untrue things), paranoia and suspiciousness about caretakers and family members, and problems with speech.
Later symptoms can include severe memory problems, difficulty eating and moving in general, loss of urinary control and speech, and severe delusions and hallucinations.
What causes it?
The short answer is that nobody knows for sure. Generally Alzheimer’s is believed to be caused by both genetic and environmental factors, with genetics possibly accounting for as much as 70% of the risk. Many different genes are involved. A poor diet, low levels of intellectual activity, cardiovascular disease, smoking, head injury, and Down’s syndrome are associated with an increased risk of Alzheimer’s.
What happens during it?
As mentioned, Alzheimer’s leads to the loss of neurons and synapses (conjunctions between neurons that allow the electrical signal to pass from one neuron to another) in the cerebral cortex.
Technically, Alzheimer’s is a protein folding disorder, because it is characterized by the accumulation of abnormally folded beta amyloid protein in the brain. Beta amyloid is normally part of a transmember protein, which penetrates the cell membrane and is critical to the growth, survival, and repair of the neuron. In Alzheimer’s, this bigger protein breaks down leaving beta amyloid, which consequentially forms clumps called plagues that accumulate outside the neuron. These plagues are characteristic to Alzheimer’s and can easily be seen with microscope in the brain of someone afflicted.
Another feature of Alzheimer’s is the accumulation of hyperphosphorylated tau protein inside the neuron. Cells have an internal “skeleton” consisting of proteins that support the cell and guide nutrients to where they are needed. Phosphate needs to be added to these proteins, and the protein tau helps with this. In Alzheimer’s, the protein tau becomes hyperphosphorylated, which means that phosphate is attached to all the sites in the protein that phosphate can attach to. Tau then starts to pair with other proteins and forms neurofibrillary tangles, disabling the transport system of the cell. These tangles can also be detected with microscope.
It is believed that, fundamentally, beta amyloid is the cause of Alzheimer’s. Experimenting has led researchers to think that it isn’t the plagues themselves that underlie the loss of neurons: rather, it’s the toxic clumps formed by only a few beta amyloid proteins. These clumps, called oligomers, attach to receptors (proteins on the surface of a neuron’s cell membrane, whose job it is to receive messages from outside) and disable them. This leads to the loss of communication between cells.
Remember the big transmembrane protein that breaks down leaving beta amyloid? Well, beta amyloid isn’t the only products of this. Right next to beta amyloid in the bigger protein is a protein called N-APP. Cells have “death receptors”: old or not useful cells are often instructed to “commit suicide”, and this happens through the activation of a death receptor. A persuasive theory suggests that, in fact, symptoms of Alzheimer’s are caused when N-APP attaches to the death receptors of neurons and that way kills the cells.
How can it be treated?
Unfortunately, an effective treatment for Alzheimer’s remains to be discovered. Medication, at best, manages to slightly relieve symptoms but not the underlying cause. Therapy may help with some symptoms and also make it easier to adjust to life with the disease. Currently the most important part of treatment is caregiving, adjusted to the patient’s personal needs and the stage of their illness. Placing safety locks, labeling items, and maintaining simple routines, for example, can improve the safety and quality of life of the patient.
Lots of scientists believe that the treatment of Alzheimer’s will come down to simultaneously aiming at many different targets with many different medications. Alzheimer’s is the target of rigorous research around the world, and while there hasn’t yet been a breakthrough, many studies have shown promising results. There is hope, and it might just be a matter of time until we find something that not only alleviates the symptoms but also affects the cause.