Alzheimer’s disease is a progressive neurological disorder that affects the brain, causing a decline in memory, thinking skills, and behavior. It is the most common cause of dementia, accounting for 60-80% of cases.

In this article, we will explore how the brain becomes affected by Alzheimer’s disease and the various changes that occur.

Neurofibrillary Tangles and Amyloid Plaques

One of the hallmark features of Alzheimer’s disease is the presence of abnormal protein deposits in the brain. These deposits include neurofibrillary tangles and amyloid plaques.

Neurofibrillary tangles are twisted fibers composed of a protein called tau. Normally, tau helps maintain the structure and function of neurons.

However, in Alzheimer’s disease, tau becomes abnormal and forms tangles, leading to disruptions in communication between brain cells.

Amyloid plaques, on the other hand, are clumps of beta-amyloid protein that accumulate between neurons.

Beta-amyloid is normally broken down and eliminated, but in Alzheimer’s disease, it accumulates and forms plaques, further disrupting brain cell activity.

Neuron Damage and Cell Death

As Alzheimer’s disease progresses, the accumulation of neurofibrillary tangles and amyloid plaques leads to damage and death of neurons in several regions of the brain.

The hippocampus, a region crucial for memory formation, is one of the first areas affected by Alzheimer’s. As neurons in the hippocampus degenerate, individuals experience difficulty with forming new memories and remembering recent events.

As the disease spreads, other regions of the brain involved in cognitive functions, such as language, attention, and problem-solving, also become affected.

This widespread neuron damage and death are responsible for the progressive decline in cognitive abilities seen in Alzheimer’s disease.

Inflammation and Oxidative Stress

In addition to the accumulation of abnormal proteins and neuron damage, inflammation and oxidative stress play a role in the progression of Alzheimer’s disease.

Inflammation occurs as a response to the accumulation of amyloid plaques and the body’s attempts to clear them. However, chronic inflammation can further contribute to neuronal damage and accelerate the progression of the disease.

Oxidative stress, on the other hand, occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to neutralize them.

ROS damage cells and can lead to further inflammation and neuronal death in Alzheimer’s disease.

Disruption of Neurotransmitters

Neurotransmitters are chemical messengers that allow communication between neurons. In Alzheimer’s disease, there is a disruption in the balance of several neurotransmitters.

Acetylcholine, a neurotransmitter involved in learning and memory, is particularly affected in Alzheimer’s. The loss of acetylcholine-producing neurons contributes to memory impairment and other cognitive deficits.

Other neurotransmitters, such as serotonin and dopamine, which play crucial roles in mood regulation and cognition, may also be imbalanced in individuals with Alzheimer’s disease.

Brain Shrinkage and Enlarged Ventricles

As Alzheimer’s disease progresses, the brain undergoes physical changes and structural abnormalities. One of the significant changes observed is brain shrinkage, also known as atrophy.

The hippocampus, as mentioned earlier, is one of the first regions to undergo atrophy in Alzheimer’s disease. As the disease progresses, other areas, including the cerebral cortex, also shrink.

This widespread brain atrophy contributes to the progressive decline in cognitive abilities.

In addition to brain shrinkage, individuals with Alzheimer’s disease may also have enlarged ventricles. Ventricles are fluid-filled spaces in the brain, and their enlargement is thought to be a consequence of the loss of brain tissue.

Genetic Factors and Alzheimer’s

While there is no single gene that causes Alzheimer’s disease, certain genetic factors can increase an individual’s risk of developing the condition.

One of the strongest genetic risk factors is the presence of the apolipoprotein E (APOE) ε4 allele. Individuals who inherit this allele from one or both parents have an increased risk of developing Alzheimer’s disease.

Other genes, such as presenilin 1 and presenilin 2, can also play a role in early-onset Alzheimer’s disease, which typically manifests before the age of 65.

Conclusion

Alzheimer’s disease is a complex neurological disorder that affects the brain in various ways. From the accumulation of abnormal proteins to neuron damage and inflammation, the disease leads to cognitive decline and memory loss.

Understanding the mechanisms through which the brain becomes affected by Alzheimer’s is crucial for the development of effective treatments and interventions.