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Am J Neurodegener Dis 2012;1(1):49-59

Original Article
Relationship of neighboring tissue and gliosis to α-synuclein pathology in
a fetal transplant for Parkinson’s disease

Tae-Beom Ahn, J William Langston, Venkat Raghav Aachi, Dennis W Dickson

Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA; Department of Neurology, School of Medicine, Kyung
Hee University, Seoul, Korea; The Parkinson Institute, Sunnyvale, CA, USA.

Received April 13, 2012; accepted April, 2012; Epub April, 2012; published May 30, 2012

Abstract: Background: Fetal transplantation for Parkinson disease (PD) had been considered a promising therapeutic
strategy; however, reports of Lewy bodies (LBs) and Lewy neurites (LNs) in engrafted tissue adds to controversy
surrounding this treatment for PD. Methods: The brain of a PD patient who had fetal transplantation 14 years before
death was evaluated.  The graft was studied with routine histologic methods, as well as immunohistochemistry for α-
synuclein, neurofilament, synaptophysin and tyrosine hydroxylase (TH), as well as glial fibrillary acidic protein (GFAP)
for astrocytes and ionized calcium-binding adaptor molecule 1 (IBA-1) for microglia. Results: On coronal sections of
the brain, the graft extended from the putamen to the amygdala, abutting the anterior hippocampus.  Microscopically,
the graft consisted of neuron-rich and glia-rich portions.  Neuron-rich portions, resembling a neuronal heterotopia,
were located in the putamen, whereas the glia-rich portion was more ventral near the amygdala.  LBs and LNs were
detected in the ventral portion of the graft, especially that part of the graft within the amygdala.  Areas with LBs and LNs
also had astrogliosis and microgliosis.  TH positive neurons were rare and their distribution did not overlap with LBs or
LNs. Comments: LBs and LNs were detected in the transplanted tissue with α-synuclein immunohistochemistry.  
Unexpected outgrowth of the graft into the amygdala was accompanied by skewed distribution of LBs and gliosis,
more abundant in the graft within the amygdala.  The distribution of LBs within the graft may suggest the potential role
of the local environment as well as gliosis in formation of α-synuclein pathology. (AJND1104001)

Keywords: Fetal transplantation, Parkinson disease (PD), therapy, α-synuclein pathology, gliosis


Address all correspondence to:
Dennis W.  Dickson, M.D.
Neuropathology Laboratory
Mayo Clinic
4500 San Pablo Road
Jacksonville, FL 32224
Phone: 904-953-7137
Fax: 904-953-7117
E-mail: dickson.dennis@mayo.edu