18 research outputs found
Are heat shock proteins an important link between type 2 diabetes and Alzheimer disease?
© 2020 by the authors. Licensee MDPI, Basel, Switzerland. Type 2 diabetes (T2D) and Alzheimer’s disease (AD) are growing in prevalence worldwide. The development of T2D increases the risk of AD disease, while AD patients can show glucose imbalance due to an increased insulin resistance. T2D and AD share similar pathological features and underlying mechanisms, including the deposition of amyloidogenic peptides in pancreatic islets (i.e., islet amyloid polypeptide; IAPP) and brain (β-Amyloid; Aβ). Both IAPP and Aβ can undergo misfolding and aggregation and accumulate in the extracellular space of their respective tissues of origin. As a main response to protein misfolding, there is evidence of the role of heat shock proteins (HSPs) in moderating T2D and AD. HSPs play a pivotal role in cell homeostasis by providing cytoprotection during acute and chronic metabolic stresses. In T2D and AD, intracellular HSP (iHSP) levels are reduced, potentially due to the ability of the cell to export HSPs to the extracellular space (eHSP). The increase in eHSPs can contribute to oxidative damage and is associated with various pro-inflammatory pathways in T2D and AD. Here, we review the role of HSP in moderating T2D and AD, as well as propose that these chaperone proteins are an important link in the relationship between T2D and AD
Inflamation and oxidative stress : The molecular connectivity between insulin resistance, obesity and Alzheimer\u27s disease
Type 2 diabetes (T 2 DM), Alzheimer’s disease (AD), and insulin resistance are age-related conditions and increased prevalence is of public concern. Recent research has provided evidence that insulin resistance and impaired insulin signalling may be a contributory factor to the progression of diabetes, dementia, and other neurological disorders. Alzheimer’s disease (AD) is the most common subtype of dementia. Reduced release (for T 2 DM) and decreased action of insulin are central to the development and progression of both T 2 DM and AD. A literature search was conducted to identify molecular commonalities between obesity, diabetes, and AD. Insulin resistance affects many tissues and organs, either through impaired insulin signalling or through aberrant changes in both glucose and lipid (cholesterol and triacylglycerol) metabolism and concentrations in the blood. Although epidemiological and biological evidence has highlighted an increased incidence of cognitive decline and AD in patients with T 2 DM, the common molecular basis of cell and tissue dysfunction is rapidly gaining recognition. As a cause or consequence, the chronic in flammatory response and oxidative stress associated with T 2 DM, amyloid- ! (A ! ) protein accumulation, and mitochondrial dysfunction link T 2 DM and AD
Economic policy in central and eastern Europe : unit root consequences. (Polityka gospodarcza w Europie Środkowo-Wschodniej: konsekwencje pierwiastków jednostkowych)
This article aims to provide an econometric justi cation for economic policy in
the Central and Eastern European area by examining the stability of real GDP and industrial
production in the Czech Republic, Slovakia, Poland, and Hungary. Stability of GDP and
industrial production is examined by unit root tests. The Dickey-Fuller (1979) unit root
test indicates unit root in case of all four outputs. In case of the industrial production, the
results are mixed. Nonetheless, difference stationarity of the GDP implies that there is no
deterministic time trend in GDP. Therefore, there is no short-run trend reversion. Deep and
long recessions are not only possible but also even likely. Thus, actions of economic policy
can be regarded as justi ed because they are desirable to boost economy in order to reverse
these recessions. This study can also be regarded as an extension of unit root tests to the
post communist countries