Why Was President Lincoln Clumsy?


For the past 16 years, people who are related to Abraham Lincoln have been meeting with researchers from the University of Minnesota to provide DNA samples and to reveal more about the Lincoln family’s medical history. These meetings have been taking place in Indiana, Iowa, and Kentucky.

 These researchers have been focusing on a disorder called ataxia within the Lincoln family. Ataxic patients are loosely defined as “anyone with clumsiness and a lack of coordination due to cerebellar degeneration.” Researchers have been able to find a number of genetic defects leading to many different forms of ataxia. However, the type of ataxia found within the Lincoln family was fairly mild. Lincoln family members affected with this type of ataxia retained their mobility longer, lived longer, and suffered less severe cerebellar degeneration. Since 1992, the Minnesota researchers have studied more than 300 members of the Lincoln family. About one-third of them have ataxia.

The “Little Brain”

The cerebellum (Latin for ‘little brain’) is an area of the brain located in the back, above the neck. The cerebellum connects the brain to the spinal cord and itself has very specific functions with a focus on motor control. The strongest clues to the function of the cerebellum have come from examining the consequences of damage to it. Animals and humans with cerebellar dysfunction show, above all, problems with motor control. They continue to be able to generate motor activity, but it loses precision, producing erratic, uncoordinated, or incorrectly timed movements. A standard test of cerebellar function is to reach with the tip of the finger for a target at arm’s length: A healthy person will move the fingertip in a rapid straight trajectory, whereas a person with cerebellar damage will reach slowly and erratically, with many mid-course corrections. Deficits in non-motor functions are more difficult to detect. Thus, the general conclusion reached decades ago is that the basic function of the cerebellum is not to initiate movements, or to decide which movements to execute, but rather to calibrate the detailed form of a movement.

Laura Rnum, PhD from the University of Minnesota-Department of Neurology began her Lincoln family gene hunt in 1992 when she received a phone call from an Ohio physician who described a patient with familial ataxia. When Dr. Ranum called the patient, as well as the patient’s mother and several cousins who were also affected with the disorder, she learned that all were related to President Lincoln. Some family members even referred to the ataxia within the extended family as “Lincoln’s disease”.

When a newspaper reporter in Louisville wrote a story about “Lincoln’s disease”, another offshoot of the family called Dr. Ranum. This time the relative was descended from President Lincoln’s Aunt Mary. The identification of this second branch of the family means that one of President Lincoln’s paternal grandparents must also have had the disease. And that, according to Ranum, means that Lincoln himself had a 25 percent chance of carrying the genetic mutation.

Locating the Defective Chromosome

In 1994 researchers from the Departments of Neurology, Laboratory and Pathology, Biochemistry, and the Institute for Human Genetics-all located within the University of Minnesota-successfully pinned down the involved gene to the 11th chromosome and named this newly discovered genetic form of ataxia SCA5 (Spinocerebellar ataxia type 5).

Spinocellebellar ataxia type 5 is one specific type of ataxia among a group of inherited diseases of the central nervous system. As in other inherited ataxias, SCA5 is caused by genetic defects that lead to impairment of specific nerve fibers carrying messages to and from the brain, resultiing in degeneration of the cerebellum-the coordination center of the brain.

SCA5 is sometimes call “Lincoln’s ataxia” because an 11-generation family with the condition has ancestries that trace to the paternal grandparents of President Abraham Lincoln. SCA5 also is called “Holmes ataxia” after Dr. Gordon Holmes, who first described the condition in 1907.

The Symptoms of SCA5

Onset of SCA5 typically is marked by an unusual stance, stumbling, difficulty climbing stairs, and losing balance while standing on one foot. Ataxia of the hands and arms also is common in SCA5, although this usually is not as disabling as the gait ataxia. Affected individuals might notice deterioration in handwriting, fastening buttons, and other activites tht require finger dexterity.

Dysarthic, slurred speech also is common, although this usually is not severe and the articulation problems are not significant enough to interfere with spoken communication.

SCA5 tends mainly to affect the cerebellum, but not other parts of the brain. It is considered a “pure cerebellar ataxia”.

The Prognosis for SCA5

Life span is generally not shortened by SCA5. It tends to be a mild, slowly progressive form of ataxia and does not affect the effects on breathing, swallowing, bowel and bladder control, thinking and strength that some forms of ataxia may bring. The onset of symptoms for SCA5 can vary between from age 10 to 70, with a mean age of onset of 33. Those individuals with early onset of SCA5 may develop more severe symptoms over time. 

SCA5 tends mainly to affect the cerebellum, but not other parts of the brain. It is considered a “pure cerebellar ataxia”.

How SCA5 is Acquired

SCA5 is a genetic disorder, which means that it is an inherited disease. The abnormal gene responsible for this disease is passed along from generation to generation by family members who carry it. Genetic diseases like SCA5 occur when one of the body’s 30,000 genes does not work properly. (Genes are microscopic structures within the cells of our bodies that contain instructions for every feature a person inherits from his or her parents.)

SCA5 is an autosomal dominant disease, which means that individuals of either sex are equally likely to inherit the gene and develop the disease, and the gene passes directly from one generation to the next without skipping generations. Each child of a person with SCA5 has a 50 percent chance of inheriting the SCA5 gene.

The Search for the Defective Gene

The hardest part of the defective gene hunt for the research team at the Univeristy of Minnesota was yet to come. The search for this gene was particularly difficult because it fell near a tightly-packed region of chromosome 11 called a centromere. For years the researchers searched through this sticky region on chromosome 11 to find the elusive gene. In 2005 the research group found what is had been seeking: the specific mutation responsible for the Lincoln family’s ataxia.

“Any family member with the gene will develop ataxia if they live long enough,” Dr. Ranum said. “And their children have a 50 percent chance of getting it, too.”

Eventually the researchers demonstrated that the mutated gene, an accident of chemistry, affects the function of another protein, called a glutamate transporter, that normally regulates how much stimulation the brain’s neurons receive. Failure to control this stimulation leads to damaged neurons; in fact, it is what likely causes the death of the cerebellum cells. With the lose of enough of these cells, affected individuals lose progressive control of the movements of their leg, arms, and eyes.

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Many historians have long speculated that President Lincoln’s tall stature may have resulted from Marfan syndrome, a disease of the body’s connective tissue. Dr Ranum said that the family history and historical accounts of Lincoln’s gait makes it much more likelly that he suffered from ataxia. Finding the mutation in the Lincoln family allows researchers to conclusively test whether President Lincoln had the SCA5 gene.

Lincoln’s last direct descendant, Robert Todd Lincon Beckwith, died in 1985 along with genetic evidence that might have shed light on the question. But it’s possible that Abraham Lincoln’s own DNA remains available in tissue samples and on items splattered with blood after his 1865 assassination.




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4 Responses to “Why Was President Lincoln Clumsy?”

  1. Denise Davis-Miller says:

    My niece and her mother ran across this article while doing a research project for school. She found it fasinating because our family also has spinocerebellar generation. I myself feel the effects with clumsiness, and being off balance. My handwriting has also deteriorated. But by the Grace of God and having a holistic doctor, it is a slow progression. I founf this article to be most inspiring.

  2. Do you guys have a twitter fan page for Why Was President Lincoln Clumsy?? I searched for one on the internet but couldn’t come across it, I would really like to become a fan!

  3. John "JC" Colyer says:

    I have cerebellar Ataxia , they saw no genetic factors in my blood test. I am impressed that Pres Lincoln was able to function and thrive with Ataxia. I’m inspired! Thanks

  4. B. Nash says:

    Ed, you have made such an interesting and thought provoking post! I’ve never seen much information on this topic. Great job!

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