The human brain contains tens of billions of neurons—specialized cells that send and receive information through electrical and chemical signals. These neurons communicate with each other and with other parts of the body, including muscles and organs. In Alzheimer’s disease, this communication system becomes impaired. Neurons begin to malfunction, lose connections, and eventually die, leading to a significant loss of brain function.
Fundamental Biological Functions in the Brain
Neurons typically consist of three main components: the cell body, dendrites, and an axon.
- The cell body houses the nucleus, which contains genetic material that controls the cell’s activity.
- Dendrites branch out from the cell body to receive signals from other neurons.
- The axon is a long fiber that carries signals away from the cell body to other neurons.
Several vital processes keep neurons functioning:
- Communication: Neurons exchange information constantly. When stimulated, a neuron sends an electrical signal down its axon. This causes the release of neurotransmitters across the synapse—a small gap between neurons. These chemicals bind to receptors on neighboring neurons, continuing the signal. This system creates an intricate communication network. A single neuron can form thousands of synapses. Early loss of these connections is a hallmark of Alzheimer’s-related cognitive decline.
- Metabolism: Brain cells need energy to function, which they get from oxygen and glucose delivered by blood. Although it weighs only about 2% of body mass, the brain consumes roughly 20% of the body’s energy. In Alzheimer’s, the brain’s ability to take in glucose and produce energy decreases, severely affecting high-energy cells like neurons.
- Repair and Remodeling: Neurons are built to last, often living for a person’s entire life. They must constantly maintain, repair, and adjust their connections based on activity. This adaptability helps with memory and learning. The brain can also create new neurons, a process called neurogenesis. However, in Alzheimer’s, this process appears to be reduced in memory-related regions.
While neurons are critical, other brain cells also play essential roles. Glial cells, which support and protect neurons, are the most numerous in the brain. These include microglia, astrocytes, and oligodendrocytes.
- Microglia act as the brain’s immune defense and clean up debris.
- Astrocytes manage nutrients and structural support.
- Oligodendrocytes create the myelin sheath that insulates axons for faster signal transmission.
These glial cells also interact with blood vessels and help regulate the brain’s immune response. Some evidence indicates that certain glial cell responses may contribute to inflammation in the brain.
How Alzheimer’s Impacts the Brain
As people age, some brain shrinkage is normal, but neuron loss is typically minimal. In Alzheimer’s, the damage is much more extensive. Neurons stop functioning properly, lose connections, and eventually die. The disease disrupts communication, metabolism, and repair mechanisms vital to brain health.
Early in the disease, the regions responsible for memory—like the entorhinal cortex and hippocampus—are affected. As the disease progresses, areas responsible for reasoning, language, and social behavior also become impaired. Eventually, the brain is so severely damaged that a person loses the ability to function independently. In the final stages, the disease is fatal.
Key Brain Features in Alzheimer’s
Before modern diagnostic tools, Alzheimer’s could only be confirmed after death by examining brain tissue. Now, imaging techniques and biomarker tests can help identify signs of the disease in living individuals. Research continues to uncover which biological changes drive the disease and which result from it.
- Amyloid Plaques: A protein fragment called beta-amyloid forms from the breakdown of a larger precursor protein. In Alzheimer’s, beta-amyloid builds up abnormally between neurons, especially in its 42-amino-acid form, forming plaques that interfere with neuron function. Scientists are still working to understand how different forms of beta-amyloid contribute to disease progression.
- Neurofibrillary Tangles: Another key feature involves the protein tau. Inside healthy neurons, tau helps stabilize internal structures called microtubules. In Alzheimer’s, abnormal tau begins to detach, stick together, and form twisted tangles inside the cell. These tangles disrupt internal transport, harming communication between neurons.
- Recent findings suggest that beta-amyloid buildup may trigger the rapid spread of tau, contributing to brain-wide damage.
- Breakdown of Neural Networks: As neurons malfunction and die, connections between neural networks collapse. This leads to widespread shrinkage of the brain, or atrophy, most evident in advanced stages of Alzheimer’s.
- Chronic Inflammation: Malfunctioning glial cells can worsen the situation. When they fail to clear out waste and protein build-up, inflammation may develop. A protein known as TREM2 helps glial cells respond to stress, including neurodegeneration. If TREM2 doesn’t work correctly, plaques accumulate, and astrocytes may fail to clean them up. This can cause glial cells to release damaging chemicals instead, contributing to chronic inflammation.
- Vascular Contributions: People with Alzheimer’s often have vascular issues such as reduced blood flow, hardened arteries, or mini-strokes. These can lower oxygen and nutrient delivery to the brain, making damage worse. Vascular problems may also impair the blood-brain barrier, which regulates the entry of substances into the brain. When this barrier fails, it can prevent essential glucose from entering the brain and allow harmful proteins to accumulate. These disruptions may trigger further inflammation and degeneration.
How Brain Changes Affect Behavior and Abilities
Researchers are continuing to explore how Alzheimer’s-related changes affect cognition. Since early damage occurs in memory-related areas, the first signs usually involve forgetting new information. As more brain regions are impacted, problems with reasoning, language, and behavior emerge. In the late stages, brain damage is so extensive that individuals lose the ability to speak, move, or care for themselves.
