Subregional 6-[18F]fluoro-ʟ-m-tyrosine Uptake in the Striatum in Parkinson's Disease

<p>Abstract</p> <p>Background</p> <p>In idiopathic Parkinson's disease (PD) the clinical features are heterogeneous and include different predominant symptoms. The aim of the present study was to determine the relationship between subregional aromatic l-amino acid decarboxylase (AADC) activity in the striatum and the cardinal motor symptoms of PD using high-resolution positron emission tomography (PET) with an AADC tracer, 6-[¹⁸F]fluoro-ʟ-<it>m</it>-tyrosine (FMT).</p> <p>Methods</p> <p>We assessed 101 patients with PD and 19 healthy volunteers. PD was diagnosed based on the UK Brain Bank criteria by two experts on movement disorders. Motor symptoms were measured with the Unified Parkinson's Disease Rating Scale (UPDRS). FMT uptake in the subregions of the striatum was analyzed using semi-automated software for region-of-interest demarcation on co-registered magnetic resonance images.</p> <p>Results</p> <p>In all PD patients, FMT uptake was decreased in the posterior putamen regardless of predominant motor symptoms and disease duration. Smaller uptake values were found in the putamen contralateral to the side with more affected limbs. The severity of bradykinesia, rigidity, and axial symptoms was correlated with the decrease of FMT uptake in the putamen, particularly in the anterior part. No significant correlation was observed between tremors and FMT uptake.</p> <p>Conclusions</p> <p>Decrease of FMT uptake in the posterior putamen appears to be most sensitive in mild PD and uptake in the anterior putamen may reflect the severity of main motor symptoms, except for tremor.</p

The ongoing pursuit of neuroprotective therapies in Parkinson disease

Many agents developed for neuroprotective treatment of Parkinson disease (PD) have shown great promise in the laboratory, but none have translated to positive results in patients with PD. Potential neuroprotective drugs, such as ubiquinone, creatine and PYM50028, have failed to show any clinical benefits in recent high-profile clinical trials. This 'failure to translate' is likely to be related primarily to our incomplete understanding of the pathogenic mechanisms underlying PD, and excessive reliance on data from toxin-based animal models to judge which agents should be selected for clinical trials. Restricted resources inevitably mean that difficult compromises must be made in terms of trial design, and reliable estimation of efficacy is further hampered by the absence of validated biomarkers of disease progression. Drug development in PD dementia has been mostly unsuccessful; however, emerging biochemical, genetic and pathological evidence suggests a link between tau and amyloid-β deposition and cognitive decline in PD, potentially opening up new possibilities for therapeutic intervention. This Review discusses the most important 'druggable' disease mechanisms in PD, as well as the most-promising drugs that are being evaluated for their potential efficiency in treatment of motor and cognitive impairments in PD

RÜLFS CRAMP AND OTHER PAROXYSMAL DYSKINESIA

Paroxysmal dyskinesia comprise a significant and fascinating part of movement disorders, which represent a diagnostic challenge for neurologists working on the borderlands of psychiatry and epilepsy. The current classification based on the relation of attacks to a movement is supported by the response to treatment and genetic difference. We reviewed clinical characteristics and the main advances in genetics of these unique, usually hereditary diseases. Clinical diagnosis remains the key to the treatment choice. Psychogenic causes are common in sporadic cases, but paroxysmal dyskinesia secondary to systemic or primary neurological disorders should not be missed and warrant careful investigation

Thrombocytopenia in HIV-infection

Determination of the number of platelets in HIV-infected people who applied in the Samara Regional Center for Prevention and Control of AIDS and infectious diseases. Thrombocytopenia was detected in 79%, severe in 23,1%. It was recorded at any stage of HIV infection and correlated with the level of CD4 lymphocytes. 45 patients was performed sternal puncture. Morphological evaluation of bone marrow showed changes in 87% of HIV-infected The most common violation was the low content or absence of megakaryocytes in bone marrow (72,5%)

IMMUNE PARAMETERS IN PATIENTS WITH BREAST CANCER AFTER RADIOTHERAPY AND SURGICAL TREATMENT

Abstract. Some immune parameters (cell subsets in peripheral blood, spontaneous and LPS-induce production of IL-1β, IL-5, IL-7, IL-12, IL-13, IL-17, G-CSF, MCP-1 and MIP-1β in whole blood cultures) were studied in fifty patients with breast cancer (T2-3, N0-3, M0) after radiation therapy and surgical treatment. A significant decrease in lymphocytes, CD3+ and CD4+T-cell counts, CD19+B-lymphocytes, erythrocytes, hemoglobin level, and amounts of phagocytic cells was revealed. The cytokine status was characterized by prevalence of pro-inflammatory cytokines (IL-1β, IL-12, IL-17) and chemokines (MCP-1, MIP-1β), accompanied by low levels of Th2/ anti-inflammatory IL-13. Furthermore, a markedly increased production of G-CSF and IL-7 was found, thus apparently pointing to the switching of a compensatory mechanisms in response to cytoreductive effects of anti-tumor therapy. IL-7 levels in lymphopenic patients (&lt; 1.2 х 109/L; a mean of 0.81±0.11) were significantly higher than that in an opposite group of lymphopenia-free women (&gt; 1.2 х 109/L; a mean of 1.34±0.01). An inverse correlation (rS = –0,88; p &lt; 0,0001) between blood lymphocyte counts and IL-7 levels allows us to suggest a mechanism of homeostatic peripheral expansion (HPE) to be involved in maintenance and restoration ofT cell homeostasis in the patients treated for breast cancer. Significance of HPE mechanism for induction of both beneficial protective tumor-specific autoimmunity and increased risk of autoimmune complications is discussed