Further Observations on the Pathology of Kuru<sup>*</sup>

Kakulas, B. A.; Lecours, Andre-Roche; Gajdusek, D. Carleton

doi:10.1097/00005072-196701000-00007

Cited by 32 publications

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“…This investigation resulted in what may be considered the definitive report of the neuropathology of kuru (Kakulas et al 1967). In this work we were able to show that the severity of the lesions was greatest in the limbic lobes of the brain and in the vermis of the cerebellum, thus demonstrating a very strong clinical correlation between the lesions and the symptoms.…”

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confidence: 99%

Personal reflections on the neuropathology of kuru

Kakulas

2008

Phil. Trans. R. Soc. B

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My involvement with kuru began towards the end of 1963 while I was a Fellow at the Massachusetts General Hospital (MGH). During the autumn of that year I was contacted by Dr Michael Alpers, who was on his way to Boston from the National Institutes of Health (NIH) in Bethesda, Maryland with a carload of New Guinean artefacts to be delivered to the Peabody Museum in Salem, Massachusetts on behalf of Dr Carleton Gajdusek. We had been students together at Adelaide University and St Mark's College in the 1950s and our friendship was thus rekindled.Sometime after this I was approached by representatives of NIH to investigate the Parkinsonism-dementia (PD) and amyotrophic lateral sclerosis (ALS) neurological complex prevalent on Guam, where it was the main cause of death among the Chamorro people. At that time, the cause of this devastating neurological complex was subject to a great deal of conjecture. These discussions led to visits to Bethesda, where I met Carleton and Joe Gibbs. This was at the exciting time when the first chimpanzees developed symptoms of kuru. Lifetime friendships were thus established with Carleton and Joe and with Jake Brody, as well as with Dr Asao Hirano in New York, who was the first to describe the neuropathology of the Guam disorders.As I was committed to the University of Western Australia, being on leave from an academic post in the medical school and feeling that I had a mission to set up neuropathology in my home country, I was not able to pursue the very attractive Guam opportunity and returned to Perth in 1965.However, earlier in that year, while deeply involved in a very busy schedule at Harvard Medical School working with my mentor in muscle diseases Dr Raymond D. Adams, Chief of Neurology at MGH, I was approached by an enthusiastic French-Canadian neurologist André-Roche Lecours. He told me about two kuru brains that had been cut in serial section at the Warren Museum of Harvard Medical School under the watchful eye of the distinguished developmental neuroscientist Dr Paul Yakovlev. Roche had concluded that I had the expertise to study and report on the two brains in association with him.At this time I had a large number of research projects going as well as being Chief Resident in Neuropathology under Dr Pierson Richardson at MGH, so I had no time at all for such painstaking work. Nevertheless, Roche prevailed and we both gave up our Sunday mornings for

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confidence: 99%

Personal reflections on the neuropathology of kuru

Kakulas

2008

Phil. Trans. R. Soc. B

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“…Astroglial hypertrophy, amyloid bodies, intra-axial orientated tubules, spiral filaments, filagree arrangements, have all been found in the scrapie-kuru-Jakob-Creutzfeldt complex (reviewed by Field, 1969.) The suggestion that kuru and scrapie, despite admittedly widespread 'non-specific' changes are essentially 'system diseases' affecting the cerebellar system (and in scrapie, too, the neuro-hypophysical complex) (Beck et al, 1964;Beck and Daniel, 1965) has received little support as more and more studies have emphasized the widespread character of the changes (Kakulas et al, 1967). The notion that scrapie is essentially a disease of the central nervous system has not gone unchallenged.…”

Section: B Pathological Changesmentioning

confidence: 99%

Scrapie: a review of its relation to human disease and ageing.

Field¹

1976

Journal of Medical Genetics

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“…There have been few pathological reports in the literature on kuru (Klatzo, Gajdusek & Zigas, 1959;Fowler & Robertson, 1959;Neumann, Gajdusek & Zigas, 1964;Kakulas, Lecours & Gajdusek, 1967); these have established the fact that the disease is confined to the nervous system and is a subacute, degenerative condition. We ourselves have investigated thirteen cases of kuru; four male and nine female, with ages ranging from 41 to 30 years (average 14j years); the duration of the illness varied between 5 and 131 months (Beck & Daniel, 1965: Beck, Daniel & Gajdusek, 1965.…”

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confidence: 99%

Degenerative diseases of the central nervous system transmissible to experimental animals

Beck

Daniel

1969

Postgraduate Medical Journal

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Summary The clinical features and the pathological changes in the central nervous system of scrapie and kuru are described and attention is drawn to the similarities between these conditions. In both, inoculation of tissues into experimental animals reproduces a similar disease after a prolonged latent period. The transmission of subacute presenile polioencephalopathy to a chimpanzee is noted. The work which led to the discovery of the transmissibility of these conditions is mentioned.

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Further Observations on the Pathology of Kuru^*

Cited by 32 publications

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Personal reflections on the neuropathology of kuru

Personal reflections on the neuropathology of kuru

Scrapie: a review of its relation to human disease and ageing.

Degenerative diseases of the central nervous system transmissible to experimental animals

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Further Observations on the Pathology of Kuru*

Cited by 32 publications

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Personal reflections on the neuropathology of kuru

Personal reflections on the neuropathology of kuru

Scrapie: a review of its relation to human disease and ageing.

Degenerative diseases of the central nervous system transmissible to experimental animals

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Further Observations on the Pathology of Kuru^*