Lewy body in neurodegeneration with brain iron accumulation type 1 is immunoreactive for α-synuclein
S Arawaka, Y Saito, S Murayama, H Mori - Neurology, 1998 - AAN Enterprises
S Arawaka, Y Saito, S Murayama, H Mori
Neurology, 1998•AAN EnterprisesIn familial PD, a mutation of the α-synuclein gene has been identified. α-Synuclein also was
revealed in Lewy bodies in idiopathic PD. Lewy bodies in neurodegeneration with brain iron
accumulation type 1 (NBIA 1; Hallervorden-Spatz syndrome) were found to show
immunostaining for α-synuclein/precursor of non-A beta component of Alzheimer's disease
amyloid, indicating that α-synuclein is commonly associated with the formation of Lewy
bodies in other sporadic and familial neurodegenerative diseases apart from PD.
revealed in Lewy bodies in idiopathic PD. Lewy bodies in neurodegeneration with brain iron
accumulation type 1 (NBIA 1; Hallervorden-Spatz syndrome) were found to show
immunostaining for α-synuclein/precursor of non-A beta component of Alzheimer's disease
amyloid, indicating that α-synuclein is commonly associated with the formation of Lewy
bodies in other sporadic and familial neurodegenerative diseases apart from PD.
In familial PD, a mutation of the α-synuclein gene has been identified. α-Synuclein also was revealed in Lewy bodies in idiopathic PD. Lewy bodies in neurodegeneration with brain iron accumulation type 1(NBIA 1; Hallervorden-Spatz syndrome) were found to show immunostaining for α-synuclein/precursor of non-A beta component of Alzheimer's disease amyloid, indicating that α-synuclein is commonly associated with the formation of Lewy bodies in other sporadic and familial neurodegenerative diseases apart from PD.
American Academy of Neurology