Alzheimer’s disease is a progressive disorder that starts and develops gradually in older people. As it progresses, the brain undergoes several changes, affecting memory, language, and thinking skills.
Brain shrinkage to a certain extent is normal in healthy aging but, surprisingly, the neurons are not lost in substantial numbers. In Alzheimer’s, however, the brain shrinks significantly due to extensive damage and neuron loss. The neurons lose the connections between them, stop functioning, and die since the disease obstructs their critical processes, including communication, metabolism, and repair.
What Parts of the Brain are Affected by Alzheimer’s?
At the outset, Alzheimer’s damages the neurons in parts of the brain which are located in the temporal lobe, including the hippocampus and entorhinal cortex, both being essential for memory. Subsequently, it deteriorates the cerebral cortex even further, affecting the frontal lobe and parietal lobe, resulting in problems with intelligence, behavior, judgment, and language. In due course, the widespread damage to many other parts of the brain leads to the gradual loss of independent functioning in people with Alzheimer’s disease., requiring full time care.
What happens to the brain with Alzheimer’s?
During Alzheimer’s progression, several cellular and molecular changes occur in the brain that can be seen microscopically in an autopsy after the patient’s death. Researchers are still trying to determine which changes cause Alzheimer’s and which changes are the results of the disease. The most prominent effects on the brain 3include the formation of beta-amyloid plaques, neurofibrillary tangles, loss of neuronal connections, and cell death.
● Amyloid Plaques
The formation of beta-amyloid proteins is a hallmark of Alzheimer’s disease. They are the minute protein particles formed by the degradation of a sizeable protein, the amyloid precursor protein.
Among its several forms, beta-amyloid 42 is the most toxic of them. The formation of this naturally occurring protein forms plaques that accumulate between the brain cells, disrupting the neuronal connection and cell function. Research is still underway to clearly understand the influence the different forms of beta-amyloid proteins have on the brain during various stages of Alzheimer’s development and progression.
● Neurofibrillary Tangles
Tau protein occurs naturally in healthy brain tissue, where it binds to and stabilizes microtubules. Microtubules are a part of the neural cell structure responsible for guiding nutrients and molecules from the cell body to both the axon and dendrites. In the Alzheimer’s brain, tau proteins form abnormal accumulations known as neurofibrillary tangles due to anomalous chemical changes. These proteins detach from microtubules and form threads by adhering to other tau molecules. Eventually, these threads join together to form tangles and disrupt neuronal communication by obstructing the cellular transportation system.
Several studies suggest a complex interplay among beta-amyloid proteins, tau proteins, and various other factors. The accumulation of abnormal tau occurs in the brain regions that control memory. Beta-amyloid, on the other hand, forms plaques between the brain cells.
● Cerebral Atrophy
Another critical Alzheimer’s-related brain change is cerebral (or brain) atrophy. With the widespread damage to neurons, connections between them are lost, eventually leading to brain shrinkage. Brain volume is reduced significantly due to extensive cerebral atrophy at the final stages of the disease.
● Chronic Inflammation
Studies suggest the role of glial cells in triggering brain inflammation. These cells keep the brain debris-free, but their build-up may cause inflammation. Microglia is a form of the glial cell responsible for initiating immune response in a healthy brain and they engulf and then degrade the toxins and wastes. In Alzheimer’s brain, however, these cells do not clean up the debris and accumulated proteins, including beta-amyloid plaques. Researchers are still trying to determine the reason for the failure of microglia to perform the debris-cleaning function in Alzheimer’s. The microglia are also involved in stimulating inflammation by releasing chemicals, further destroying the neurons they are meant to preserve.
