Chemical structure consisting of oxygen, hydrogen, and nitrogen. The body requires a continuous supply of protein to meet its functional and energy needs. Proteins compose numerous substances in the body including enzymes, hormones, cell structures, and deoxyribonucleic acid (DNA). Scientists have identified a number of proteins and corresponding gene mutations that direct their functions that have roles in Parkinson’s disease. Proteins are constructed of hundreds to thousands of amino acids, the smallest units of organic structure. Although there are only about 20 amino acids, the ways in which they combine allow them to form countless proteins. DNA, a cell’s genetic code, determines how each cell synthesizes (makes) and uses proteins. The more complex the protein, the greater the likelihood of errors in its synthesis.
In the 1990s scientists identified mutations in the alpha- synuclEin GENE and the PARKIN gene in significant numbers of people with Parkinson’s disease. These genes regulate the synthesis of alpha-synuclein, a complex protein that facilitates synaptic communication among brain neurons, and a number of other proteins that scientists know are present in the brain but do not fully understand. Alpha-synuclein has been one of the most extensively studied brain protein to date. Researchers also know that the neurons often contain structures called inclusions. In the brain of people with Parkinson’s disease, these inclusions are characteristic structures called lewy bodies, which are composed primarily of alpha synuclein. The correlation between these protein-based inclusions, the role of alpha-synuclein in synaptic communication, and the neurodegenera-tion that occurs in Parkinson’s disease remains unclear.
Alzheimer’s disease was the first neurodegen-erative disease for which scientists discovered a conclusive protein connection, that of the tau protein, which forms the characteristic deposits and neurofibrillary tangles that are the pathological hallmark of Alzheimer’s. As with Parkinson’s, there are gene mutations that correspond with the apparent malfunction of tau protein synthesis. And also as with Parkinson’s, the correlation of tau, the deposits, and the disease process in Alzheimer’s is not fully understood. Both proteins alpha-synuclein and tau are present in healthy brains, but not as deposits. People who have one of these diseases, Parkinson’s or Alzheimer’s, also have a much higher risk than other people their age of having the other, raising intriguing questions about connections between the two disease processes and the role of protein synthesis in health and in disease. Researchers are optimistic that unraveling these connections will provide crucial understanding of the causes of and possible cures for both, as well as related diseases.