Position Emission Tomography/Single-Photon Emission Tomography Neuroimaging for Detection of Premotor Parkinson's Disease.

Premotor Parkinson's disease (PD) refers to a prodromal stage of Parkinson's disease (PD) during which nonmotor clinical features may be present. Currently, it is difficult to make an early diagnosis for premotor PD. Molecular imaging with position emission tomography (PET) or single-photon emission tomography (SPECT) offers a wide variety of tools for overcoming this difficulty. Indeed, molecular imaging techniques may play a crucial role in diagnosing, monitoring and evaluating the individuals with the risk for PD. For example, dopaminergic dysfunctions can be identified by detecting the expression of vesicular monoamine transporter (VMAT2) and aromatic amino acid decarboxylase (AADC) to evaluate the conditions of dopaminergic terminals functions in high-risk individuals of PD. This detection provides a sensitive and specific measurement of nonmotor symptoms (NMS) such as olfactory dysfunction, sleep disorders, and psychiatric symptoms in the high-risk patients, especially at the premotor phase. Molecular imaging technique is capable of detecting the dysfunction of serotonergic, noradrenergic, and cholinergic systems that are typically associated with premotor manifestations. This review discusses the importance of SPECT/PET applications in the detection of premotor markers preceding motor abnormalities with highlighting their great potential for early and accurate diagnosis of premotor symptoms of PD and its scientific significance.

Progressive supranuclear palsy: what do we know about it?

Progressive supranuclear palsy (PSP) is a progressive tauopathy characterized by supranuclear ophthalmoplegia, pseudobulbar palsy, dysarthria, axial rigidity, frontal lobe dysfunction, and dementia. The typical pathology includes neuronal loss, gliosis and microtubule-associated protein tau (MAPT)-positive inclusions in neurons and glial cells, primarily in basal ganglia, brainstem and cerebellum. The pathogenesis of PSP is not yet completely understood; however, there are several hypotheses. This article reviews the present knowledge about PSP, and the concepts underlying mitochondrial dysfunction, lipoperoxidation, and gene mutations. The clinical features of PSP are also discussed; these include vertical gaze palsy, pseudobulbar palsy, aphasia, dysarthria, axial rigidity, and neuropsychiatric symptoms, such as amnesia, irritability, loss of interest, and dementia. In terms of diagnosis, there is considerable interest in neuroimaging for detecting PSP; therefore, neuroimaging techniques such as magnetic resonance imaging (MRI) and [18F]- fluorodeoxyglucose positron-emission tomography (FDG-PET) are reviewed. A definitive diagnosis of PSP depends on pathology, and the introduction of new clinical subtypes challenges presents the widely adopted diagnosis criteria. PSP treatments such as serotonin antagonists, α2 receptor antagonists, and coenzyme Q10 are also discussed. There is no curative therapy for PSP; all of the available treatments are palliative.