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BrainFacts.org

Creation Date: 16 Jan 2010 | Review Date: 16 Jan 2010

Unraveling Alzheimer's Disease

Source: Society for Neuroscience

Whether it is a grandparent, older relative, or friend, most people know someone who is affected by Alzheimer’s disease. Brains afflicted with Alzheimer’s disease degenerate as the cells that carry information disappear. As a result, patients with the disease, usually the elderly, suffer memory loss and cognitive impairment. This disease is a significant problem across the globe, and as populations grow and life expectancies rise, the number of people suffering from Alzheimer’s disease may skyrocket. However, new research is helping to identify its cause and is pointing the way to potential treatments that may help delay the onset of this devastating neurological disorder.

Image of a brain with Alzhimer's disease
As Alzheimer’s disease progresses, it kills brain cells mainly in the hippocampus and cortex, which leads to impairments in learning, memory, and thinking.
Adapted and reprinted with permission from the Alzheimer’s Association. © 2008 Alzheimer’s Assocation.

Imagine what would happen if you forgot the names of your parents. Or if you suddenly realized you had no idea where you were, or what time it was. Although everyone experiences some memory loss as they age, significant disruptions that impair day-to-day life are cause for concern and may be signs of Alzheimer’s disease. 

Diseases like Alzheimer’s most commonly occur in the elderly, causing significant memory loss and other cognitive difficulties. Symptoms of Alzheimer’s disease include forgetfulness; disorientation to time and place; and difficulty with concentration, calculation, language, and judgment. 

According to the Alzheimer’s Association, one in eight people over the age of 65 develops Alzheimer’s disease. It affects more than 40 percent of people over age 85 and nearly 20 percent of those ages 75 to 84. Increasing life spans and a growing world population mean that we can expect to see a rise in the number of individuals who will develop this disease. With Alzheimer’s disease predicted to affect approximately 14 million people in the United States alone by 2040, unraveling the biology of this disorder is all the more important.  

We are learning more about the causes of Alzheimer’s disease and are researching new ways to help treat and delay its onset. Ongoing research is helping us:

  • Learn about the biological causes of Alzheimer’s disease by studying new clues from cell biology and genetics.
  • Identify health conditions and lifestyle factors that can increase or decrease the risk of Alzheimer’s disease.

Many researchers are examining the protein deposits that form in Alzheimer’s disease brains for clues about the disorder’s underlying cause. Alzheimer’s disease brains contain hard, insoluble plaques, which are made of large deposits of a protein called beta-amyloid. The plaques themselves were once believed to be responsible for disrupting brain cell communication; however, recent research has suggested that different forms and smaller amounts of beta-amyloid may be to blame. New research in animal models of Alzheimer’s disease gives hope that treatments targeting beta-amyloid may prevent or delay disease progression. 

Alzheimer’s disease brains also include deposits of the tau protein that are called tangles because of their fibrous appearance. Like amyloid plaques, these protein clumps may be at the heart of the Alzheimer’s disease process. Researchers are now looking for ways to limit protein build-up and tangle formation. 

Advances in genetics are helping to identify people most at risk for developing Alzheimer’s disease and the molecules and cellular processes that help to cause the disease. Researchers have identified three genes (APPPSEN1 and PSEN2) that cause early-onset Alzheimer’s disease, which strikes before the age of 65. Although scientists agree that several genes likely contribute to increased risk for the more common, later onset form of the disease, only one gene (APOE) is currently known to do so. Researchers are now investigating how APOE is involved in the Alzheimer’s disease process. 

Scientists are also identifying medical conditions and lifestyle factors that affect the risk of Alzheimer’s disease and activities that might slow its progress. For example, people with Type 2 diabetes may be at increased risk of developing Alzheimer’s disease. Damage to the blood vessels that supply the brain may also increase Alzheimer’s disease risk. Together, these findings suggest that maintaining healthy weight, blood pressure, and cholesterol may reduce the risk for Alzheimer’s disease. 

Additional research suggests that Alzheimer’s disease may kill brain cells by hijacking a process involved in normal brain development. During development, the brain makes too many brain cell connections. Like overgrown trees, the ones that are not needed are “pruned” back. Researchers recently found that the larger “parent” protein that produces beta-amyloid — amyloid precursor protein — also produces a protein fragment that activates the pruning process. Deprived of their cellular connections, many mature brain cells die. This new finding suggests that Alzheimer’s disease kills brain cells by reactivating the pruning process at the wrong time, later in life. Blocking pruning might therefore be beneficial to at-risk adults. 

Researchers share a long-term goal to stop the global impact of Alzheimer’s disease and recognize that the global community offers unique opportunities for Alzheimer’s research. By studying populations with rich cultural and genetic diversity, researchers may gain new insights into the causes of the disease, specifically the genetic and lifestyle factors that protect against or enhance disease risk. 

Because Alzheimer’s disease permanently changes the brain, it is not presently seen as reversible. Is it preventable? Researchers hope discoveries will one day make prevention possible. Today, the goal is to delay the onset of the disease as long as possible because doing so would limit its impact given that it strikes late in life. Achieving any of these goals will require the efforts of a global community of scientists and clinicians as well as making funding for that research a priority around the world.  

Further Reading

Bertram L, Tanzi RE (2008) Thirty years of Alzheimer’s disease genetics: the implications of systematic meta-analyses. Nature Reviews Neuroscience 9: 768-778.

Ballatore C, Lee VMY, Trojanowski JQ (2007) Tau-mediated neurodegeneration in Alzheimer’s disease and related disorders. Nature Reviews Neuroscience 8: 663-672.

Zhao WQ, De Felice FG, Fernandez S, Chen H; Lambert MP, Quon MJ, Krafft GA, Klein WL (2008) Amyloid beta oligomers induce impairment of neuronal insulin receptors. The FASEB Journal 22: 246-260.

De Felice FG, Vieira MNN, Bomfim TR, Decker H, Velasco PT, Lambert MP, Viola KL, Zhao WQ, Ferreira ST, Klein WL (2009) Protection of synapses against Alzheimer’s-linked toxins: Insulin signaling prevents the pathogenic binding of Aß oligomers. PNAS 106(6): 1971-1976.

Nikolaev A, McLaughlin T, O’Leary DDM, Tessier-Lavigne M (2009) APP binds DR6 to trigger axon pruning and neuron death via distinct caspases. Nature 457: 981-990.

About the Author

Debra Speert
Debra manages scientific communication for the Society for Neuroscience, particularly on BrainFacts.org. While completing a PhD and postdoctoral fellowship in neuroscience, she discovered a knack for explaining tough scientific concepts to general audiences.