Affiliations: [a] Department of Neurology, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Switzerland | [b] Department of Internal Medicine, Rehabilitation and Geriatrics, Geneva University Hospitals and Faculty of Medicine, Switzerland | [c] Unit of Psychopathologic Morphology, Department of Mental Health and Psychiatry, Geneva University Hospitals and Faculty of Medicine, Switzerland
Correspondence:
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Correspondence to: Judit Horvath, M.D., Department of Neurology, Geneva University Hospitals and Faculty of Medicine, Rue Gabrielle-Perret-Gentil 4, 1211 Geneva 14, Switzerland. Tel.: +41 22 372 83 18; Fax: +41 22 372 80 99; E-mail: [email protected].
Abstract: About one third of Alzheimer's disease (AD) patients develop some parkinsonian features, yet half of them do not have Lewy body pathology at autopsy. The neuropathological substrate of parkinsonism in AD is still unclear. In the present study, we measured neuronal and neurofibrillary tangles (NFTs) densities in the substantia nigra pars compacta (SN) and in the putamen of 22 AD patients, 11 with and 11 without parkinsonism, here defined as the presence of bradykinesia and at least one of resting tremor, rigidity, or gait disorders. Our study showed that parkinsonism associated with AD was related to a significant loss of neurons both in the SN and in the putamen, suggesting pre-and postsynaptic alterations of the nigrostriatal pathway. Neuronal tau deposition was a less important factor as density of NFTs correlated with parkinsonism only in the SN but not in the putamen. We propose that a subgroup of pure AD patients develop parkinsonian symptoms as a result of neuronal loss in the basal ganglia, indicating a prominent subcortical involvement, which appears unrelated to the Braak stage of AD.
Keywords: Alzheimer's disease, histology, parkinsonism, pathology, putamen, substantia nigra
