These results demonstrated that the presence of RBD in patients with PD is associated with different patterns of both motor deficit distribution and striatal DAT depletion, suggesting that the presence of RBD represents a distinct PD subtype with a malignant motor parkinsonism.
The nigro-striatal dysfunction explored by dopamine transporter imaging is not a mandatory diagnostic criterion for Parkinson disease, recent evidence supported its utility as in-vivo proof of degenerative parkinsonisms, and there might be compensatory mechanisms leading to an early overestimation.
This review addresses the possibilities and limitations of DAT-SPECT in PD and, focusing specifically on regulatory changes of DAT in surviving DA neurons, we investigate its role in diagnosis and its prognostic value for motor complications as disease progresses.
The authors conducted a case-control study of Parkinson's disease patients with and without visual hallucinations to investigate associations of the polymorphisms of the dopamine receptors D2 32806 C>T (Taq1A), D3 Ser9Gly and Msp1, D5 978T>C and dopamine transporter 3'-UTR 40 bp VNTR with visual hallucinations in Parkinson's disease.
DAT SPECT is expected to be useful in differentiating SCA2 from Parkinson's disease, making an early diagnosis, and allowing early therapeutic intervention.
In the present review, some of the most recent and relevant achievements in the field of diffusion tensor magnetic resonance imaging (MRI), functional MRI, fludeoxyglucose-positron-emission tomography, dopamine transporter single-photon emission computed tomography and non-dopaminergic imaging in PD and primary Parkinsonisms are reported.
Additionally, all participants underwent a battery of clinical assessments to determine motor and non-motor symptoms and cognitive status, and [<sup>123</sup>I]FP-CIT single-photon emission CT (SPECT) to assess striatal dopamine transporter binding and MRI for volumetric analyses to assess whether pathology is associated with measures of Parkinson's disease burden.
The <i>ATG5</i> down-regulation led to the upgrade of PD-associated proteins, such as β-synuclein, Parkin, and PINK1, aggravation of MPTP-induced PD-mimicking pathological locomotor behavior, DA neuron loss labeled by tyrosine hydroxylase (TH) or dopamine transporter (DAT), and blocked autophagy flux in the zebrafish model.
DAT serves as a site of action for a variety of addictive and therapeutic reuptake inhibitors, and transport dysfunction is associated with transmitter imbalances in disorders such as schizophrenia, attention deficit hyperactive disorder, bipolar disorder, and Parkinson disease.
The homozygote 10-copy genotype of variable number tandem repeat dopamine transporter gene may confer protection against Parkinson's disease for male, but not to female patients.
Of the two patients with bradykinesia, DAT density was reduced to the Parkinson's disease (PD) range with a rostrocaudal gradient typical of PD in one patient (CAG repeats 13/22) and was mildly decreased in the other patient (12/25).
In a macaque model of PD, also based on delivery of AAV1/2-hourA53T-aSyn to the SN, trehalose (2.67 g/kg per day, by mouth), administered for 142 days, produced higher striatal dopamine (by 39%) and dopamine transporter levels (by 50%), compared with macaques receiving vehicle.
The coding region of the DAT gene, SLC6A3, is well conserved, but non-coding regions are more variable, most notably a variable number of tandem repeats (VNTR) polymorphism in the 3' untranslated region, which has been studied in a number of dopamine-related neurological disorders, including Parkinson's disease (PD).
However, the combination of the two genotypes 10R/10R (rs28363170) and A carrier (rs393795) of the DAT gene reduces the risk of LID occurrence during long-term therapy with l-DOPA with respect to the PD subjects who did not carry these alleles (OR = 0.31; 95% CI, 0.09-0.88).
The aromatic L-amino-acid decarboxylase (AADC) defect appears to be consistently smaller than the dopamine transporter and vesicular monoamine transporter 2 defects, suggesting upregulation of AADC function in PD.
The followings, for instance, are only a few of the many new biomarkers that have been recently identified: the phosphorylated tau protein and aggregated Beta-amyloid peptide for Alzheimer's disease (AD), Alpha-synuclein contained Lewy bodies and altered dopamine transporter (DAT) imaging for Parkinson's disease (PD), SOD mutations for familial amyotrophic lateral sclerosis (ALS), and CAG repeats resulted from Huntington's gene mutations in Huntington's disease (HD).
Twenty-six patients are reported.Three patients had dementia with Lewy bodies; one had an atypical parkinsonism; 22 had PD, including one with schizophrenia and neuroleptic exacerbated, dopamine transporter scan-positive idiopathic PD; and another had PD complicated by strokes.