Brain Changes Due to Alzheimer's Disease

Alzheimer's disease causes physical changes to the brain that affect brain functions. Brain functions are adversely affected by two types of brain lesions—amyloid plaques and tau protein "tangles"—a fact that has been well-documented by medical science. While an autopsy is currently the only way to check for Alzheimer's lesions, PET and CT scans can sometimes reveal changes in brain tissue caused by Alzheimer's disease.

 

Beta-Amyloid Protein Plaques

Beta-amyloid is a naturally occurring protein that usually causes no difficulties. Alzheimer's disease, however, is characterized by the formation of beta-amyloid protein plaques that build up in the brain and affect brain functions. The protein plaques build up between the brain neurons. Although it has not been proven, researchers speculate that plaques build up before noticeable changes to brain functions can be seen.

 

Researchers have discovered that a molecule called CCR1, which is found on the surface of white blood cells, is also associated with beta-amyloid plaques in Alzheimer's patients. CCR1 is present even in the very early stages of Alzheimer's and it's concentration increases as the disease progresses. Researchers hope the current Phase 1 clinical trials will support using CCR1 as a biological marker for early detection of Alzheimer's disease and for tracking its progression.

 

Researchers at UC Irvine have identified that beta-amyloid is responsible for the memory loss experienced in Alzheimer's. When immunotherapy was used to clear the beta-amyloid plaques from affected neurons in genetically engineered laboratory mice the mice's memory deficit was repaired. This could be an important finding as researchers attempt to develop drugs to treat Alzheimer's disease.

Tau protein is essential for normal brain functions. The protein plays a role in maintaining neuron structure. When Alzheimer's disease is present, tau protein strands twist, creating "neurofibrillary tangles." As the protein strands twist, they damage local neurons. When enough neurons are damaged by the protein lesions, brain functions become compromised.

Low levels of the neurotransmitter acetylcholine also affect brain function in Alzheimer's sufferers. Acetylcholine is necessary for memory functions as well as other cognitive functions. Maintaining acetylcholine levels is often the goal of Alzheimer's treatments, and the FDA has approved several Alzheimer's medications that help slow the decrease of acetylcholine.

Brain tissue degeneration due to Alzheimer's disease affects the cortex and hippocampus more than other areas of the brain. The cortex is important for memory recall, reasoning, and personality. The hippocampus processes new information.

 

As well as the damage caused by brain lesions, some Alzheimer's patients show evidence of brain inflammation. Immune cells may target beta-amyloid plaques or may attempt to remove cells affected by tangles. In doing so, the inflammation may further degrade brain functions.

 

Oxidation may also cause brain function degeneration. Oxidation is a form of cellular damage that increases with age. "Free radicals" cause oxidation. Free radicals are naturally occurring oxygen molecules that build up in the body throughout life. Vitamin E and other antioxidant vitamins are thought to protect brain cells from oxidation.

 

Resources

 

Billings, L.M., Oddo, S., Green, K.N., McGaugh, J.L., LaFerla, F.M. (2005, March 3). Intraneuronal Aβ causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice. Neuron 45(5), 675-688.

 

Eriksen, J.L, Sagi, S.A,, Smith, T.E., Weggen, S., Das, P., McLendon, D.C., Ozols, V.V., et al. (2003, August). NSAIDs and enantiomers of flurbiprofen target g-secretase and lower Aβ42 in vivo . The Journal of Clinical Investigation, 112(3), 440-449.

 

Lab Tests Online. (updated 2002). Tau/Aβ42 Test.