What Happens to the Brain in Alzheimer's Disease?

SUSHRUT -A Magazine of Pharmaceutical Sciences

Volume 1, Issue 1, August 2024, Pages 11-13

What Happens to the Brain in Alzheimer's Disease?

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August 2024 ➧ A MAGAZINE OF PHARMACEUTICAL SCIENCES ➧ ¹ Institute of Pharmaceutical Sciences, RKDF University, Ranchi, Jharkhand-834004, India ➧ Volume 1

Alzheimer's disrupts processes vital to neurons and their networks, including communication, metabolism, and repair. It's characterized by changes in the brain that lead to deposits of certain proteins. At first, Alzheimer's usually damages the connections among neurons in parts of the brain involved in memory, including the entorhinal cortex and hippocampus. Damage to nerve cells in the brain can also make it difficult for the person to express thoughts and perform routine tasks without assistance. Alzheimer's disease causes the brain to shrink and brain cells to eventually die. The person in the final months of Alzheimer's disease will experience increased mental and physical deterioration, eventually needing 24-hour care.

: Alzheimer, Alzheimer’s Disease, Entorhinal cortex, Hippocampus

Introduction

Alzheimer's disease primarily affects the brain by causing progressive degeneration of nerve cells, leading to cognitive decline, memory loss, and changes in behavior. The brain is our most powerful organ, yet weighs only about three pounds. It has a texture similar to firm jelly.

In the brain the cerebrum fills up most of your skull. It is involved in remembering, problem solving, thinking, and feeling. It also controls movement. The cerebellum sits at the back of your head, under the cerebrum. It controls coordination and balance. The brain stem sits beneath your cerebrum in front of your cerebellum. Alzheimer's disease profoundly affects the brain, leading to significant cognitive decline and behavioral changes. The disease primarily targets neurons, disrupting their function and eventually causing cell death. The main things of Alzheimer's disease include the accumulation of amyloid plaques and tau tangles, which interfere with neural communication and contribute to neuronal damage. As the disease progresses, it impacts various brain regions, beginning with the hippocampus, which is essential for memory formation. This leads to early symptoms like memory loss and confusion. Over time, the disease spreads to other areas of the brain, affecting functions such as language, reasoning, and spatial abilities [1].

Etiology

Amyloidal Plaques

Formation of Plaques: Alzheimer’s disease is characterized by the accumulation of amyloidbeta protein plaques between nerve cells (neurons) in the brain. These plaques disrupt cell-tocell communication. Neuronal Damage: The buildup of plaques can trigger an inflammatory response and lead to neuronal damage and death.

Neurofibrillary Tangles

Tau Protein Tangles: Another hallmark of Alzheimer’s is the formation of neurofibrillary tangles inside neurons. These tangles are composed of abnormally phosphorylated tau

proteins.

Disruption of Nutrient Transport: The tangles disrupt the transport system within neurons, which is essential for moving nutrients and other important substances within the cell. This disruption contributes to cell death.

Loss of Synapses

Synaptic Loss: Alzheimer’s leads to the loss of synapses, the connections between neurons. This loss impairs communication between neurons, affecting learning and memory.

Reduction in Neurotransmitters: There is a significant reduction in neurotransmitters, such as acetylcholine, which are crucial for memory and learning processes.

Brain Atrophy

Shrinkage of Brain Tissue: As neurons die, the brain tissue shrinks, leading to atrophy. This shrinkage is particularly noticeable in the hippocampus, which is responsible for forming new memories.

Enlarged Ventricles: The loss of brain tissue results in the enlargement of the brain's

ventricles (fluid-filled spaces) [2],[3].

Symptoms

Memory Loss: Short-term memory is typically affected first, with patients having difficulty recalling recent events. Over time, long-term memory is also impacted.

Cognitive Decline: Patients experience declines in various cognitive functions, including reasoning, problem-solving, and judgment.

Language Impairment: There is a gradual deterioration in language abilities, including difficulty finding the right words, forming coherent sentences, and understanding spoken and written language.

Mood Changes: Patients may experience mood swings, depression, and anxiety.

Behavioral Changes: Changes in behavior, such as increased agitation, aggression, and wandering, are common as the disease progresses.

Hallucinations and Delusions: In advanced stages, patients may experience hallucinations and delusions [2],[3].

Stages of Progression

Preclinical Stage: Changes in the brain begin years before symptoms appear. This stage is characterized by the accumulation of amyloid plaques and tau tangles without noticeable symptoms.

Mild Cognitive Impairment (MCI): Patients have mild but noticeable changes in memory and cognitive abilities. These changes are not severe enough to interfere significantly with daily life [2],[3].

Conclusion

The cumulative effect of these pathological changes results in the hallmark symptoms of Alzheimer's, including severe memory impairment, disorientation, and changes in behavior and personality. Ultimately, Alzheimer's disease leads to a decline in the ability to perform daily activities and requires comprehensive care and support. Research continues to seek better understanding, early detection, and effective treatments for Alzheimer's disease. Advances in these areas hold the promise of mitigating the impact of the disease and improving the quality of life for those affected and their caregiver.

References and Bibliography

1. https://www.nia.nih.gov/health/alzheimers-causes-and-risk-factors/what-happensbrain-alzheimers-disease
2. https://my.clevelandclinic.org/health/diseases/9164-alzheimers-disease
3. Bhushan I, Kour M, Kour G, et al. Alzheimer’s disease: Causes and treatment – A review. Ann Biotechnol. 2018; 1(1): 1002.