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Mitochondria and Free Radicals
Any given cell has hundreds of mitochondria. This illustration shows two—a healthy mitochondrion and an oxidatively stressed and damaged one. The arrows indicate the movement of free radicals, which can spread easily from damaged mitochondria to other parts of the cell.
老年癡呆症 (Alzheimer's disease, AD) 是威脅老年人生命的三大疾病之一
老年癡呆症 (阿茲海默症)(Alzheimer's disease, AD)
Oxidatively stressed and damaged mitochondria, and free radicals [2009-06-30](IR90) - with source URL.jpg
Protein Misfolding
Researchers have found that a number of devastating neurodegenerative diseases (for example, AD, Parkinson’s disease, dementia with Lewy bodies, frontotemporal lobar degeneration, Huntington’s disease, and prion diseases) share a key characteristic—protein misfolding.
When a protein is formed, it “folds” into a unique three-dimensional shape that helps it perform its specific function. This crucial process can go wrong for various reasons, and more commonly does go wrong in aging cells. As a result, the protein folds into an abnormal shape—it is misfolded. In AD, the misfolded proteins are beta-amyloid (the cleaved product of APP; see "From APP to Beta-Amyloid Plaques" for more on the formation of beta-amyloid) and a cleaved product of tau.
Normally, cells repair or degrade misfolded proteins, but if many of them are formed as part of age-related changes, the body’s repair and clearance process can be overwhelmed. Misfolded proteins can begin to stick together with other misfolded proteins to form insoluble aggregates. As a result, these aggregates can build up, leading to disruption of cellular communication, and metabolism, and even to cell death. These effects may predispose a person to AD or other neurodegenerative diseases.
Scientists do not know exactly why or how these processes occur, but research into the unique characteristics and actions of various misfolded proteins is helping investigators learn more about the similarities and differences across age-related neurodegenerative diseases. This knowledge may someday lead to therapies.
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The Aging Process
Another set of insights about the cause of AD comes from the most basic of all risk factors—aging itself. Age-related changes, such as inflammation, may make AD damage in the brain worse. Because cells and compounds that are known to be involved in inflammation are found in AD plaques, some researchers think that components of the inflammatory process may play a role in AD.
Mitochondria and Free Radicals
Any given cell has hundreds of mitochondria. This illustration shows two—a healthy mitochondrion and an oxidatively stressed and damaged one. The arrows indicate the movement of free radicals, which can spread easily from damaged mitochondria to other parts of the cell.
Other players in the aging process that may be important in AD are free radicals, which are oxygen or nitrogen molecules that combine easily with other molecules (scientists call them “highly reactive”). Free radicals are generated in mitochondria, which are structures found in all cells, including neurons.
Mitochondria are the cell’s power plant, providing the energy a cell needs to maintain its structure, divide, and carry out its functions. Energy for the cell is produced in an efficient metabolic process. In this process, free radicals are produced. Free radicals can help cells in certain ways, such as fighting infection. However, because they are very active and combine easily with other molecules, free radicals also can damage the neuron’s cell membrane or its DNA. The production of free radicals can set off a chain reaction, releasing even more free radicals that can further damage neurons (see illustration "Mitochondria and Free Radicals"). This kind of damage is called oxidative damage. The brain’s unique characteristics, including its high rate of metabolism and its long-lived cells, may make it especially vulnerable to oxidative damage over the lifespan. The discovery that beta-amyloid generates free radicals in some AD plaques is a potentially significant finding in the quest for better understanding of AD as well as for other neurodegenerative disorders and unhealthy brain aging.
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