- Brain illnesses
There's no animal model for the human brain
It’s a simple argument to claim that monkeys have similar brains to humans. Monkeys have similar bodies, and behaviour with some similarities. But this isn’t enough to justify studying the monkey brain to learn about human brains. The way illness develops in complex organs like the brain means that the details with which we study in medicine aren’t available in non-humans.
Monkeys have complex brains, but not nearly as complex as a human brain. Research shows that a monkey brain develops in 136 days, yet a human brain takes 470 days to develop, a period which exceeds the gestation period . The monkey brain has about 10% of the surface area of a human brain. Neurons are cells that make connections; in human they make 7-10,000 connections, but in rhesus monkeys the connections number 2-6,000. The genetic activity is vastly different, and already 91 genes involved in neurological processes are known to have different effects . The human brain has areas connected with vision that do not exist in monkeys .
As a primate researcher admitted “the human brain …is more than simply a large monkey or ape brain.” 
Another criticised animal research, saying: “...today the neurological theatre or the clinical investigation unit is in fact a superbly equipped laboratory, with the important advantage that its experiments are carried out on man rather than the guinea-pig.” 
This might be expected to be recent, following the incredible imaging techniques made available over the last decade. But this quote is from Medical Journal The Lancet from 1971, indicating that for many years it’s been clear that animal experiments have not been the best method. In reality, medical research on the brain has depended on human study, not animals.
Animal experiments of Traumatic Brain Injury (TBI) are also acknowledged to be ineffective, as reported in a July 2010 medical journal:
“So why have TBI trials been so unsuccessful? In addition to poor classification of patients going into trials, like many other diseases it comes down to inadequate animal models. Rats have strikingly different brains than humans, and it may be that some brain injury mechanisms important in rats are not so important in humans or vice versa. Amyloid deposits, a neurotoxin that has been shown to aggregate in the brain of some TBI patients as well as Alzheimer’s patients, simply don’t form in rat models of TBI...At the University of Cambridge, David Menon no longer studies brain injury in lab animals, but sticks to human data. “The failure of [clinical trials] suggests that we are obviously getting something wrong, so it was quite important to make the change,” says Menon.”
AD was identified in humans at autopsy using microscopes, when it was found that a protein left deposits on the brain (now called neurofibrillary tangles). The protein exists in mice, and much time and money has been spent altering it in mice – although this mice involved had no AD symptoms.
There are no effective animal models: “The full spectrums of the biochemical and pathological abnormalities characterized by AD have not been found to occur spontaneously in any animal species other than human…” 
Another expert explains: “There is no good animal model for the disease process characterized by a loss of cognitive functions and memory decline.”
They lack the most basic characteristics: “More problematically, these animals do not develop neurofibrillary tangles or show significant neurodegeration.”
“Alzheimer's, Parkinson's and other neurodegenerative diseases occur in humans and it is in human tissue that we will find the answers to these diseases.” 
MS is caused by the immune system attacking itself, and the cause is not yet known. Animal tests have centred around EAE, an animal model, which “is totally different clinically, immunologically and histologically from MS” . It has also been described as “not acceptable as a model for MS for many reasons” 
Animal models have misled experimenters about how MS progresses. They have also provided numerous potential drug treatments, which have failed:
“Time after time, researchers have discovered new ways to cure laboratory rats of experimental induced encephalomyelitis, the murine [mouse] model of MS, only to face obstacles in bringing the treatment to humans” .
“A large number of potential MS therapies have been envisaged from experiments in animals...it should be stressed that the application of these potential therapeutic techniques to humans has been consummately associated with failure” .
Treatments developed on animals include Tumor necrosis factor (which has the opposite effect in humans) , Copaxone (which came with numerous side effects) , and injected immunoglobins, which were no more effective than placebos . Peptide ligand formulas trials were abandoned as patients nearly died .
The failure has been noted: “Experimental allergic encephalomyelitis is not a suitable animal model for testing treatments for multiple sclerosis and it is time to explore alternative experimental and therapeutic approaches.” 
Clinical research and cell-culture work using T-cell lines and cells taken from individual patients has been the basis for effective research.
To see the new research which has made massive impact on the MS world in late 2010, click here.
John Hughlings Jackson identified that the cause of epilepsy is abnormal electrical brain discharges. This was through studying patients, although these days we have the advantages of EEG technology to study patients in more detailed ways.
Cell culture and computer technology has been invaluable: “The detailed models for focal interictal discharges arose largely from experiments on brain slices in vitro [studied after death], combined with computer simulations.” 
Technology, not animal testing, has been the method of progress, and this is not disputed. A meeting of animal research supporters identified the most important methods as: brain imaging methods (especially MRI), surgical technique and the ability to detect opportunities for surgery, and molecular genetics. Animal experiments were not mentioned.
Dr Med. Bernhard Rambeck, Director of the Biochemistry Department of the Society for Epilepsy Research in Bielefield-Bethel, Germany stated:
“As a scientist, I am of the opinion that animal experiments bring no progress in the diagnosis and therapy of epilepsies. I have a well-founded suspicion that similar facts apply in other areas of medicine.” 
High profile campaigns by the animal testing lobby would imply that progress in treating PD is a good example of the benefits of animal research. There are no good animal models for PD. The most widespread way is to apply a harsh chemical to the brain of primates, which causes, temporary, slight loss of function, which can be reversed – not like humans.
“The best model of PD to date, is the…(MPTP)-lesioned marmoset….unlike human PD, which is progressive, the neurotoxic damage produced by MPTP is reversible.”
PD was never really understood until 1960. An Austrian team discovered through autopsy that a degeneration of a specific part of the brain caused PD.  Human studies followed which confirmed the importance of the neurotransmitter dopamine and led to use of Levodopa to stimulate dopamine levels.
Surgical techniques have been used, such as removing the thalamus. A newer technique is Deep Brain Stimulation (DBS) which enables patients to control the condition by operating electrodes implanted in the brain. Claims have been made that this technique was made possible my primate brain experiments, but the reality was very different.
Electrodes are used to affect neurons to aid surgical technique in thalamotomies. By chance, a French doctor used the wrong frequency and found that this calmed the neurons, and tried applying them to other parts of the brain. This suggested that it may stop PD symptoms. Later he attempted the technique in a patient and was successful.
Read more about Parkinson's Disease here.
Other illnesses have been the subject of high profile claims in favour of animal testing. Read the reality here.
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