Given the enormous morbidity and mortality associated with these devastating diseases, the potential impact of vitamin D supplementation at a population level is staggering and is certainly worthy of further investigation in well-designed clinical trials. G. D and G. E. conceived the idea of the review. G. D., S. K., J. K., S. R., and G. E. drafted the manuscript and critically reviewed the content. G. D. is supported by the AANF/CMSC

John F. Kurtzke Clinician-Scientist Award, a Goodger Scholarship (University of Oxford), and the NIHR Biomedical Research Centre, Oxford. None. “
“Tauopathies are clinically, morphologically, and biochemically PD0325901 mouse heterogeneous neurodegenerative diseases characterised by the deposition of abnormal tau protein in the brain. The neuropathological phenotypes are distinguished based on the involvement of different anatomical areas, cell types and presence of distinct isoforms of tau in the pathological deposits. The nomenclature of primary tauopathies overlaps with the modern classification of frontotemporal lobar degeneration. Neuropathological phenotypes comprise Pick`s disease, progressive supranuclear palsy,

corticobasal degeneration, argyrophilic grain disease, primary age-related tauopathy (PART), formerly called Navitoclax solubility dmso also as neurofibrillary tangle-only dementia, and a recently characterised entity called globular glial tauopathy. Mutations in the gene encoding the microtubule associated protein tau (MAPT) are associated with frontotemporal dementia and parkinsonism linked to chromosome 17. In addition, further neurodegenerative conditions with diverse aetiologies may be associated with tau pathologies. Thus the spectrum of tau pathologies and tauopathy entities expands beyond the traditionally discussed disease-forms. Detailed FAD multidisciplinary studies are still required understand their significance. “
“Since cystatin C (CysC) in involved in some forms of neurodegeneration, we investigated

the possible relationship between CysC and multiple system atrophy (MSA), including its parkinsonian (MSAp) and cerebellar (MSAc) phenotypes. Cystatin C gene (CST3) haplotypes were determined by PCR followed by KspI digestion in 50 MSA patients and 108 controls. CST3 and cathepsins B, D and L1 mRNA levels were studied in frozen post-mortem caudate nucleus and cerebellar samples of 8 MSAp, 4 MSAc and 18 control brains and analyzed by the deltadeltaCt method. CysC immunohistochemistry was performed on 3 MSAp, 3 MSAc and 3 control cerebella. Additionally, determination of CST3 and cathepsins B, D and L1 mRNA levels and immunohistochemistry for CysC were carried out in cerebella from 3 patients with paraneoplastic cerebellar degeneration, 3 with spinocerebellar ataxia (type 3, SCA3) and 3 with cerebellar ischemia (CI). In the set of blood samples, the CST3 B-haplotype was associated with MSAp (OR 4.86, CI 1.84-13.3).