This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Winner, B. Articles by Winkler, J. Search for Related Content Social Bookmarking                   What's this?

Review: Cellular repair strategies in Parkinson's disease

Department of Neurology, University of Regensburg, Regensburg, Germany, Salk Institute of Biological Studies, La Jolla, CA, USA

Daniela M. Vogt-Weisenhorn

Institute for Developmental Genetics, Helmholtz Zentrum München German Research Center for Environmental Health, Neuherberg, Germany

Chichung D. Lie

Institute for Developmental Genetics, Helmholtz Zentrum München German Research Center for Environmental Health, Neuherberg, Germany

Ingmar Blümcke

Department of Neuropathology, University Hospital Erlangen, Schwabachanalge 6 DE - 91054 Erlangen, Germany, ingmar.bluemcke @uk-erlangen.de

Jürgen Winkler

Department of Neurosciences, University of California San Diego, La Jolla, CA, USA, Division of Molecular Neurology, University Hospital Erlangen, Erlangen, Germany

Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease, affecting 0.7% of the elderly population (defined as over 65 years of age). PD is clinically characterized by resting tremor, muscular rigidity, hypokinesia and postural instability. These motor symptoms result largely from the deficiency or dysfunction of dopaminergic neurons in the substantia nigra. Histopathological analysis reveals depletion of dopaminergic neurons as well as eosinophilic intracytoplasmic inclusions (Lewy bodies) in surviving neurons of the substantia nigra and other brain regions. The molecular pathogenesis is linked to protein misfolding by compromised alpha-synuclein and/or related proteins (synucleinopathy). Therefore, successful therapy of motor symptoms aims for the restoration of dopaminergic neurotransmission. Pharmacological drug treatment is usually effective only at an early stage of the disease but cannot halt progressive neuronal degeneration. With recent developments in stem cell technology, cell repair or replacement approaches came into focus. Here, we review new therapeutic strategies resulting from the innate propensity of the adult brain to generate new neurons, either by pharmacological stimulation of endogenous adult stem cell population or exogenous cell transplantation modalities.

Key Words: stem cells • neurogenesis • transplantation • neurodegeneration • alpha-synuclein

Therapeutic Advances in Neurological Disorders, Vol. 2, No. 1, 51-60 (2009)
DOI: 10.1177/1756285608100324


CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?