α-synuclein is a protein that plays important roles in cognitive function in the normal brain, although its exact role is not fully understood. However, current studies reveal that defects in α-synuclein function could contribute to various neurodegenerative disorders, such as Parkinson’s disease (PD), a disease with symptomatic progression of deterioration in motor and cognitive function. Recent studies show that the level of α -synuclein in cerebrospinal fluid (CSF) is highly correlated with speed of cognitive decline, suggesting a potential role of α-synuclein in cognitive function. In this mini review, we will be focus on literatures of α-synuclein in cognitive function in the non-diseased brain, as well as the impact that defective α-synuclein has on cognition in disease brain. This will be accomplished by assessing the effects of soluble α-synuclein, α-synuclein oligomers, and extracellular α-synuclein transport, on neurodegeneration.
Fetal neurology is a new challenging field. Brain damage often originates in fetal life. Early identification of this damage has implications for perinatal management; moreover documentation of such lesions is essential in case of litigation. In the last two decades, fetal imaging with 2-dimensional ultrasounds and conventional magnetic resonance imaging have made a major contribution in the identification of classic brain lesions and malformations. However, it is only recently with diffusion weight imaging that the whole spectrum of perinatal white matter injuries has been described in the neonate. The recent advances of 3DUS and 4DUS in exploring fetal motor behavior should support a better clinical description of the full spectrum of fetal damage. New neurological test (KANET) of the fetus recently suggested by us (Kurjak et al 2008) might be helpful in the assessment of fetal neurobehavior.
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