Alzheimer’s disease (AD) affects 5 million people in the United States, according to the Alzheimer’s Association. The progressive disease disrupts memory and thinking. It also impairs and eventually kills brain cells.
This impairment can lead to symptoms that include:
- difficulty with time
- language problems
- inability to recognize loved ones
In AD, a protein called beta-amyloid shows up in irregular clumps or clusters in the brain. This protein comes from a precursor protein found in a fatty membrane that covers nerve cells.
The clumps of beta-amyloid fragments stick together to form plaque. These sticky clusters interrupt signals between synapses. Synapses are the spaces between nerve cells where information passes from one cell to another.
Scientists still aren’t certain whether beta-amyloid plaque causes AD, or whether the irregular clusters in the brain result from the disease process.
Researchers are also still sorting out whether clumped or unclumped versions of beta-amyloid cause AD.
Researchers do know that mutations in APP, the precursor protein that forms beta-amyloid plaque, causes early onset AD.
In normal brain tissue, a protein called tau stabilizes microtubules. Microtubules are key parts of cell structure.
In a diseased brain, protein strands, or threads, become tangled. As a result, the brain system of transporting cell nutrients along parallel structures — which can be compared to railroad tracks — falls apart.
Without these critical nutrients, brain cells die.
Memory and thinking depend on the transmission of signals across 100 billion neurons in the brain.
AD interferes with this cell signal transmission. It also affects the activity of brain chemicals called neurotransmitters.
The scrambled chemistry produces flawed signaling, so the brain’s messages are lost. This impacts the ability to learn, remember, and communicate.
Microglia are a type of cell that initiate immune responses in the brain and spinal cord. When AD is present, microglia interpret the beta-amyloid plaque as cell injury.
The microglia go into overdrive, stimulating inflammation that further damages brain cells.
Some AD research focuses on how this inflammatory response can be reduced or controlled.
In advanced AD, the surface layer that covers the cerebrum, the largest part of the brain, withers and shrinks. This damage to the cortex plays havoc with the brain’s normal ability to plan ahead, recall, and concentrate.
Alzheimer’s disease also affects the hippocampus, which plays an important role in memory. The disease causes the hippocampus to shrivel. This harms the brain’s ability to create new memories.
Unfortunately, there is no cure for AD. However, certain treatments like behavioral therapy and medication can help ease symptoms of the disease.
Some medications may help to ease symptoms of confusion and memory loss. These include cholinesterase inhibitors and memantine, which are sometimes used together.