Biomedical subjects

Marcin Flirski

Publications and source records attributed to Marcin Flirski.

4 recordsLinked to original sources

PubMed2005

Biochemical markers and risk factors of Alzheimer's disease.

As the spectrum of therapeutic options broadens, the possibility of an early and accurate diagnosis of Alzheimer's disease (AD), or even isolation of a group at high risk of subsequent cognitive decline, is focusing widespread attention. Therefore, biological markers or risk factors of AD are highly desirable. In this work, we give an overview of the most extensively studied AD biomarkers, namely beta-amyloid, tau protein, and phosphorylated tau-protein, alone or in combination. Moreover, we describe the role of inflammatory markers (cytokines, acute phase proteins), oxidative stress markers (isoprostanes, 8-hydroxyguanine, 3-nitrotyrosine, plasma antioxidants, redox transition metals), homocysteine and related vitamins, cholesterol and 24S-hydroxycholesterol in the diagnostic process or prediction of AD. We briefly review less popular, though promising markers of AD - markers of apoptosis, neuronal thread protein, acetyl- and butyrylcholinesterase, sulfatide, kallikreins, matrix-degrading metalloproteinases, and novel isoforms of beta-amyloid and tau. Finally, we discuss the clinical applicability of AD-related biological markers.

Alzheimer Disease↗

PubMed2005

Plasma levels of alpha beta peptides are altered in amnestic mild cognitive impairment but not in sporadic Alzheimer's disease.

Plasma alpha beta levels have been examined in sporadic Alzheimer's disease yielding conflicting results; both no difference and an increase in plasma concentrations of alpha beta42 and alpha beta40 in sporadic cases of AD as compared to controls have been reported. Elevated plasma alpha beta42 levels may be detected several years before the onset of symptoms (in mild cognitive impairment stadium). Levels of alpha beta40 and alpha beta42 were measured in plasma from 54 patients with AD, 39 subjects with MCI and 35 controls using a commercially available ELISA. Mean plasma alpha beta42 levels were significantly higher in MCI as compared to both AD (P < 0.001) and control subjects (P < 0.001), while alpha beta40 did not differ between the groups. No correlations were observed between alpha beta levels and age, MMSE scores or gender. According to ROC curve analysis the maximum accuracy in discriminating MCI versus both controls and AD subjects has been achieved using a cut-off value of 3.8.

Aged↗

PubMed2004

Amyloid-beta and tau proteins as biochemical markers of Alzheimer's disease.

With the development of new therapeutic strategies, and the concept of mild cognitive impairment (MCI) as an early stage of Alzheimer's disease (AD), there is an increasing need for an early and accurate diagnosis of sporadic AD. Therefore, biological markers allowing a positive diagnosis early in the course of the disease are highly desirable. The most extensively evaluated markers of sporadic AD are amyloid-beta proteins and levels of both total and phosphorylated microtubule-associated protein tau. In this study, we review the currently available data on the aforementioned markers assessed in the cerebrospinal fluid or plasma, alone and in combinations, focusing on their clinical applicability including sensitivity in the diagnosis of AD and mild cognitive impairment, specificity in discriminating AD from other dementias and correlations with the disease progression and apolipoprotein E genotype. We also analyze advantages and potential drawbacks of using biomarkers in the laboratory diagnosis of AD.

Alzheimer Disease↗

PubMed2004

Doppel: the prion's double.

Doppel (Dpl) is a PrP-like protein, coded by a gene named PRND, located near the PRNP (prion proten coding gene) locus. Human Dpl is a 179-amino acid protein showing approximately 25% sequence identity with the carboxyproximal two thirds of the human cellular prion protein (PrPC). A comparison of the structures of Dpl and PrP(C) reveals similarities in the secondary structure and topology. Apart from their structural similarities, the PrP and Dpl proteins seem to have different functions. The Prnd gene is expressed in mouse embryos; in adult mice its transcripts are present in heart, mammary gland, spleen, testes and, in contrast to Prnp, only at very low levels in the adult CNS. Moreover, the Dpl protein is not capable of enhancing the propagation of the pathological prion protein (PrP(Sc)). The Dpl protein has been identified as a regulator of acrosome function and male gametogenesis. The human PRND open reading frame has been shown to contain polymorphic codons, but research on a correlation between the PRND polymorphic sequences and neurodegenerative disorders carried out to date in different populations have shown contradictory results. Therefore, the role of the PRND gene in CJD and other diseases still remains unexplained.

Animals↗