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Neurotoxicity of a prion protein fragment
TLDR
It is reported here that neuronal death results from chronic exposure of primary rat hippocampal cultures to micromolar concentrations of a peptide corresponding to residues 106–126 of the amino-acid sequence deduced from human PrP complementary DNA.
Synthetic amyloid-β oligomers impair long-term memory independently of cellular prion protein
TLDR
It is reported that, in mice, acute intracerebroventricular injections of synthetic Aβ1–42 oligomers impaired consolidation of the long-term recognition memory, whereas mature Aβ 1–42 fibrils and freshly dissolved peptide did not, and it was confirmed that A β1– 42 oligomers interact with PrPC, with nanomolar affinity.
An N-terminal Fragment of the Prion Protein Binds to Amyloid-β Oligomers and Inhibits Their Neurotoxicity in Vivo*
TLDR
N1, the main physiological cleavage fragment of the cellular prion protein, is necessary and sufficient for binding early oligomeric intermediates during Aβ polymerization into amyloid fibrils and strongly suppresses Aβ oligomer toxicity in cultured murine hippocampal neurons, in a Caenorhabditis elegans-based assay, and in vivo in a mouse model of Aβ-induced memory dysfunction.
TMEM106B regulates progranulin levels and the penetrance of FTLD in GRN mutation carriers
TLDR
TMEM106B SNPs significantly reduced the disease penetrance in patients with GRN mutations, potentially by modulating GRN levels, and hold promise for the development of future protective therapies for FTLD.
Identification of prion protein gene polymorphisms in goats from Italian scrapie outbreaks.
Susceptibility to scrapie in sheep is influenced by polymorphisms of the prion protein (PrP) gene, whereas no strong association between genetics and scrapie has yet been determined in goats due to
Homocysteine, folate, and vitamin B-12 in mild cognitive impairment, Alzheimer disease, and vascular dementia.
TLDR
Findings suggest that relative folate deficiency may precede AD and VaD onset and Hyperhomocysteinemia might also be an early risk factor for cognitive decline in the elderly, but its role in dementia development must be addressed in future longitudinal studies.
Full length alpha-synuclein is present in cerebrospinal fluid from Parkinson's disease and normal subjects.
TLDR
Full length alpha-synuclein is released by neurons in the extracellular space and does not appear a peripheral marker of PD pathology, which has two implications.
Evaluation of Quinacrine Treatment for Prion Diseases
TLDR
Despite its ability to cross the blood-brain barrier, the use of quinacrine for the treatment of CJD is questionable, at least as a monotherapy, and the multistep experimental approach employed here could be used to test new therapeutic regimes before their use in human trials.
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