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Brain, Vol. 125, No. 1, 44-57, January 1, 2002
© 2002 Oxford University Press

Two large British kindreds with familial Parkinson’s disease: a clinico-pathological and genetic study

D. J. Nicholl*,1, J. R. Vaughan*,2, N. L. Khan2, S. L. Ho7, D. E. W. Aldous1, S. Lincoln8, M. Farrer8, J. D. Gayton5, M. B. Davis2, P. Piccini3, S. E. Daniel4, G. G. Lennox6, D. J. Brooks2,3, A. C. Williams1 and N. W. Wood2

1Department of Neurology, Queen Elizabeth Hospital, Birmingham, 2Institute of Neurology, Queen Square, 3MRC Clinical Sciences Unit, Imperial College School of Medicine, Hammersmith Hospital, 4Parkinson’s Disease Society Brain Research Centre, Wakefield Street, London, 542, Hyde Street, Winchester, 6Department of Neurology, Addenbrooke’s Hospital, Hills Road, Cambridge, UK, 7Division of Neurology, University of Hong Kong, Hong Kong and 8Department of Pharmacology, Mayo Clinic Jacksonville, Jacksonville, Florida, USA Correspondence to: Dr David J. Nicholl, Department of Neurology, Queen Elizabeth Hospital, Birmingham B15 2TH, UK E-mail: d.j.nicholl{at}bham.ac.uk

*These authors contributed equally to this work

We present the findings of a study of two large unrelated kindreds with autosomal dominant Parkinson’s disease. The affected members were assessed clinically and with [18F]6-fluorodopa-PET and were indistinguishable from patients with the sporadic form of Parkinson’s disease. In one kindred, an affected member was examined subsequently at autopsy and Lewy bodies were present in a distribution typical of sporadic Parkinson’s disease. These kindreds are distinct from other Parkinsonian kindreds with identified genetic loci (PARK1–4) and provide further evidence for genetic heterogeneity in familial Parkinson’s disease.


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