Stephen Mullin

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α-Synuclein (SNCA) is a substantive component of Lewy bodies, the pathological hallmark of Parkinson’s disease (PD). The discovery and subsequent derivation of its role in PD has led to a suprising but fruitful convergence of the fields of biochemistry and molecular genetics. In particular, the manipulation of the cell lines of a number of forms of familial(More)
Acute porphyria, though rare, has well-known neurological sequelae. Vasospasm rarely complicates exacerbations of acute intermittent porphyria, but has not been previously reported in hereditary coproporphyria. We describe a porphyric crisis in a woman with previously undiagnosed hereditary coproporphyria (triggered by rifampicin), leading to vasospasm and(More)
The last 2 decades represent a period of unparalleled advancement in the understanding of the pathogenesis of Parkinson disease (PD). The discovery of several forms of familial parkinsonism with mendelian inheritance has elucidated insights into the mechanisms underlying the degeneration of dopaminergic neurons of the substantia nigra that histologically(More)
The conversion of α-synuclein from its intrinsically disordered monomeric state into the fibrillar cross-β aggregates characteristically present in Lewy bodies is largely unknown. The investigation of α-synuclein variants causative of familial forms of Parkinson disease can provide unique insights into the conditions that promote or inhibit aggregate(More)
PRIMARY OBJECTIVE Increasing support exists for the development of post-traumatic stress disorder (PTSD) after traumatic brain injury (TBI). Despite the psychological nature of PTSD, previous reviews have mainly focused on the injury-related and neurological characteristics of its presentation in TBI. Consequently, this review systematically examined the(More)
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