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Decreased concentration of Annexin V in Parkinsonian cerebrospinal fluid: Speculation on the underlying cause
Author(s) -
Vermes Istvan,
Jansen Steur Ernst N.H.,
Reutelingsperger Chris,
Haanen Clemen
Publication year - 1999
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/1531-8257(199911)14:6<1008::aid-mds1015>3.0.co;2-e
Subject(s) - cerebrospinal fluid , annexin , programmed cell death , apoptosis , endocrinology , medicine , parkinson's disease , dopaminergic , ex vivo , neuroscience , disease , chemistry , biology , dopamine , in vitro , biochemistry
Circumstantial evidence suggests that increased apoptosis is responsible for the loss of dopaminergic nigrostriatal neurons in Parkinson's disease (PD). It is impossible to perform high‐quality studies on human postmortem material because of the low quality of tissue preservation, and the fact that apoptosis has a duration of only hours, and that the duration of the agonal period itself will lead to massive neuronal cell death. We measured, as epiphenomenon of neuronal cell death ex vivo, the Annexin V concentration in cerebrospinal fluid (CSF) in patients with PD and control subjects. The Annexin V concentration in CSF of patients with PD was significantly lower compared with control subjects. Annexin V concentrations of the CSF did not correlate with dementia, duration of symptoms, age, sex, or treatment of PD. The rationale for measurement of Annexin V in CSF is the fact that Annexin V adheres to dying cells. It is tempting to suppose that the decrease of Annexin V in CSF of PD is the result of consumption of this protein during neuronal apoptosis as has been demonstrated to occur in the midbrain in PD.