What is Alzheimers disease Ivan Seah Yu Jun

Every four seconds,

someone is diagnosed with

Alzheimer’s disease.

It’s the most common cause of dementia,

affecting over 40 million people worldwide,

and yet finding a cure is something that still

eludes researchers today.

Dr. Alois Alzheimer, a German psychiatrist,

first described the symptoms in 1901

when he noticed that a particular hospital patient

had some peculiar problems,

including difficulty sleeping,

disturbed memory, drastic mood changes,

and increasing confusion.

When the patient passed away,

Alzheimer was able to do an autopsy

and test his idea that perhaps

her symptoms were caused by irregularities

in the brain’s structure.

What he found beneath the microscope

were visible differences in brain tissue

in the form of misfolded proteins

called plaques,

and neurofibrillary tangles.

Those plaques and tangles work together

to break down the brain’s structure.

Plaques arise when another protein

in the fatty membrane surrounding nerve cells

gets sliced up by a particular enzyme,

resulting in beta-amyloid proteins,

which are sticky and have a tendency

to clump together.

That clumping is what forms the things

we know as plaques.

These clumps block signaling

and, therefore, communication

between cells, and also seem to trigger

immune reactions that cause the destruction

of disabled nerve cells.

In Alzheimer’s disease, neurofibrillary tangles

are built from a protein known as tau.

The brain’s nerve cells contain a network of tubes

that act like a highway for food molecules

among other things.

Usually, the tau protein ensures that these tubes

are straight, allowing molecules

to pass through freely.

But in Alzheimer’s disease,

the protein collapses into twisted strands or tangles,

making the tubes disintegrate,

obstructing nutrients from reaching the nerve cell

and leading to cell death.

The destructive pairing of plaques and tangles

starts in a region called the hippocampus,

which is responsible for forming memories.

That’s why short-term memory loss

is usually the first symptom of Alzheimer’s.

The proteins then progressively invade

other parts of the brain,

creating unique changes that signal

various stages of the disease.

At the front of the brain,

the proteins destroy the ability to process logical thoughts.

Next, they shift to the region that controls emotions,

resulting in erratic mood changes.

At the top of the brain,

they cause paranoia and hallucinations,

and once they reach the brain’s rear,

the plaques and tangles work together

to erase the mind’s deepest memories.

Eventually the control centers governing

heart rate and breathing are overpowered as well

resulting in death.

The immensely destructive nature of this disease

has inspired many researchers to look for a cure

but currently they’re focused on slowing its progression.

One temporary treatment

helps reduce the break down of acetylcholine,

an important chemical messenger in the brain

which is decreased in Alzheimer’s patients

due to the death of the nerve cells that make it.

Another possible solution is a vaccine

that trains the body’s immune system to attack

beta-amyloid plaques before they can form clumps.

But we still need to find an actual cure.

Alzheimer’s disease was discovered

more than a century ago,

and yet still it is not well understood.

Perhaps one day we’ll grasp

the exact mechanisms at work behind this threat

and a solution will be unearthed.