CA = Cerebellar Abiotrophy. Previously called Cerebellar Hypoplasia until it was discovered that the latter develops in the embryo/fetus and the foal is born with degenerated Purkinje Cells. With CA, the degenration occurrs after birth , initiating aproximately 30 days post birth. The rate of degeneration varies and whereas most foals with this neurological condition can display clinical signs at 3 or 4 months of age, there have been many cases which were not recognized until 18 months to 3 years. There was a case in 2006 where a six year old mare which had been backed and ridden for two years previously with no problems unexpectedly appeared with CA. Her blood was pulled , tested and carried markers. She was euthanized and a brain sample sent to UC Davis for a histopathic diagnosis. It was positive. This was a very unusual case.

Cerebellar Abiotrophy is NOT a Lethal Disease. It does not kill the foal/horse.

In many ways it is worse

With a total lack of balance and no spatial conception. The foal is lucky to survive the repeated accidents it will be having. The usual running, bucking, rearing and jumping that all foals participate in as youngsters can end up impaled on a fence, and/or with head injuries & concussions, back injuries from bad falls, and a general "stay-away-from-it" attitude from the herd in general. (As horses are herd orientated animals, this is bad). If the foal survives weaning and continues to grow up without a major accident to itself or to a handler, by the time it is 3 years old, it must face training which often is the time and the person who sees that there is a serious problem. Cross ties, even a single tie can be lethal for the CA affected horse. So is trimming and shoeing. Some can not even tolerate fly sprays , much less being trimmed because it startles them so much that they panic. The more stressed they become, the worse their condition is expressed.

Affected CA horses can not be ridden or driven safely. They need a tremendous amount of patience and work even to be trailered. They will get to learn the parameters of their environment and hence appear to be improving but they are not. Change them to a new field or stable and they will be back to ground zero again, having to learn by trial and error all over again. 800 lbs. + of adult horse can do a lot of damage to itself and whatever it runs in to. Including You.

These horses should not be bred. In fact , many of them physically can not be bred. They can not stand up without falling over. So what does the breeder/owner do if he/she can not keep the horse for the next 20 years as a pasture pet? They have lost the time. They have lost the stud fee. They have lost maintenance and vet fees and worse if they own either the dam or the sire, they know for sure that they have a CA Carrier. Not to mention the sadness, frustration, and total helplessness.

Responsible breeders/owners euthanize.
Irresponsible breeders/owners sell the horse onward if they can or give it away. What happens to the horse? Maybe it will be lucky for a few years. Most will end up being passed from one owner to another and eventually end up in a deplorable starving negligent condition. Some of the lighter cases are even bred with AI and of course all their progeny will be 100% carriers and with a likelihood that a few of those foals will also be affected.

I would rather have a foal with a Lethal condition like scid. You lose all the same things but at least you know that it all will be over by 4 or 5 months ...even sooner if you suspect the condition early and send in samples for testing.

Having a foal with CA is worse than having one with scid.
CA is a lifelong horror story.

Make your breeding selections carefully. Test your breeding stock. Ask if the stallion you want to bred to , has been tested.

It is found basically in purebred Arabians and is beleived to exist in all bloodline groups, some breeds with Arabian crosses, the miniature horse; is well known amongst certain breeds of cats and dogs and some breeds of cows and pigs. Wikipedia has a full coverage article at Cerebellar Abiotrophy with many online links.

There has been much discussion on the subject on public forums and some of the owners have confirmed Carrier information. As well, some of the documentary literature which has been published in medical journals has designated highly suspect bloodlines. As a monogenic autosomal recessive form of inheritance, CA has been in the Arabian gene pool for generations, back to the original desert breeding. It is so widespread throughout all the Arabian bloodlines across the world that it *has* to come from the original Bedouin stock. Witchhunts & finger pointing is not necessary. The acceptance that it does exist in all Arabian bloodlines IS. This condition has been acknowledged since the 1840s and undoubtedly was known about, if only verbally, prior to that time.

An indepth article which discusses publicly acknowledged status of lines and affected horses can be found here:

It is important to understand that Carriers can and will produce Clear progeny. These individuals will breed onwards and if not bred to another carrier, will continue to remain clear. This is why some well-known and popular lines continue onwards in present day. If any horses should have crosses to suspected lines, they should be tested.

With a recessive, a mutant allele can pass onward ''unexpressed" for generations. Line Breeding and Inbreeding enhances the possibility of expression and the more times a Carrier line or individual appears in the background of a pedigree, the greater the odds that an affected foal will be produced.

N/N = Normal (clear)
CA/CA = Affected
N/CA = Carrier

N/N x N/N = Clear 100%
N/N x N/CA = Clear 50%, Carrier 50%, Affected 0%
N/CA x N/CA = Clear 25%, Carrier 50%, Affected 25%.

If a slightly affected and unrecognized horse is used for breeding : (which happens)
N/N x CA/CA = Clear 0%, Carrier 100%, Affected 0%.
N/CA x CA/CA = Clear 0%, Carrier 50%, Affected 50%.

There is an indirect genetic test developed for establishing carriers and non-carriers of Cerebellar Abiotrophy now available at UC Davis under the direction of Dr. Cecilia Penedo and her research team.

For those who are wondering how there can be a test when the specific mutant allele has not be identified as yet, the following video ( 59 minutes) is self explanatory. I have posted a synopsis of the clip as the video is long and may be difficult for dial up members to download.

I did find it to be a very good explanation of the Horse Genome, how the "Markers" are calculated and how this knowledge is applied to a diagnostic analysis.

VIDEO: (Video is third on the list and one has to sign up/register to view - free no fee)

SPEAKERS:James N. MacLeod, VMD, Ph.D. (Gluck Equine Research Center)
Ernie Bailey, Ph.D. (Gluck Equine Research Center)
Teri Lear, Ph.D. (Gluck Equine Research Center)

Presented at the University of Kentuckyʼs Livestock Disease Diagnostic Center in conjunction with the Department of Veterinary Sciences.

SYNOPSIS: Until 1990, sophisticated machinery was not in place to do any DNA sequencing. 3 billion dollars went into developing the right kind of sequencing machines to sequence the HUMAN GENOME and over thirty of these were built.

That started the roll so to speak and as the years went by while developing the Human Genome ( completed in 2004), the machinery were improved and constantly updated. Thus by 2006 after a royal battle to include "Horses" in the selected but limited species of mammals to be sequenced, equines were finally approved of , instead of only zebras and rhinoceros which were the original representatives of the same branch.

Originally it was thought that horses had multiple millions of genes, as in 100 million. By 1990 only 20 genes were identified in the horse and those were thought to be a mere 2 % of the total. Then it was discovered that all mammals have aproximately 20, 000 only. It turns out that the horse has 20,737 genes.

With this new DNA sequencing process, to the tune of $25 million dollars to complete the Horse Genome (pronounced G-Nome) , 21 billion base pairs of DNA were sequenced. This made available 1.47 million genetic variants of 'Single Nucleotide Polymorphisms' on record. These variants are called SNPs (pronounced snips). This obviously is a pretty huge base for data research. The result is 60,000 identifiable markers.

Until recently these markers had to be collected from families _ sire, dam, offspring. It is now found that the markers can be collected from the same breed of horse and still have the same value. A huge step in genetic research findings.

How to scientists develop Markers?
- By using 20 horses with a known condition and 20 horses known not to have the condition. DNA is pulled; transferred to the workable RNA for slide and synapse sequencing. These are machine tested against the 60,0000 known Identified markers.
- All Markers will be identical in all 40 specimans used, EXCEPT for those horses which carry the defective or undesirable gene.

The examples given were to trace horses with desirable hoof quality and horses with non-desirable hoof quality. The results with these new DNA sequencing machines show a very distinct and reliable difference in the gentic make up (Markers) of horses with bad hooves and those with good quality hooves. With a genetic disease, the results show those horses with normal Markers and those horses without the normal Markers. Each sample contains 20 to 30 million '"Tags" of '35 Base pair Sequence' reads. These are all thrown up on a comparative graph and must be processed. Each test for the total SNPs, run aproximately $12,000 per run which is why there is no great rush to get them done...lack of funds.

As all Markers will be identical within the same breed of horse, it is possible to segregate those horse samples which do not have 100% identical Markers to the known healthy specimens.

With all CA affected or Carrier horses having similar Markers which are not found in the healthy test group, the attributes of the 'wild' gene are identified and recorded. (As it is known that the cerebellum is the only causative area, the research studies are regulated to this tissue for comparative studies.)

This enables the indirect diagnostic testing of hair follicle samples to establish the fact whether a horse is a CA Carrier or not, even though the specific mutated allele is not identified as to "name' or exact location. All of which means that the current indirect diagnostic testing supported by UC Davis is as accurate as can be expected.

The public announcement that World Champion  MARAJJ is a carrier of Cerebellar Abiotrophy has come as a shock to many but is also a giant step forward for Arabian breeders.

The Albidayer Stud and owner Sheikh Mohammed Bin Saud Al Qasimi is to be congratulated for disclosing the status of MARAJJ on their website in Latest News Updates on 2 December 2008.        Please visit their website for more information.

Owners interested in having horses screened for the CA markers, can request the test directly from the Veterinary Genetics Laboratory (VGL) at UC Davis through the following website
VetGen also offers the test at a reduced price in conjunction with testing for SCID.  This is available through this site ( on the Test Kits page.

For assistance with ordering the test online, contact the VGL’s Customer Service section by phone (530) 752-2211, FAX (530) 752-3556 or email (

A special thank you to Lisa Goodwin-Campiglio  of Spain for submission of the above material including its links.

Purkinje Cells Birth to 90 Days               Purkinje Cells Microphotography