A Recent Update on the Role of Estrogen and Progesterone in Alzheimer's Disease.

Alzheimer's disease (AD), one of the most prevalent neurodegenerative disease responsible for 60%-80% dementia cases globally. The disease is more prevalent among elder females. Female reproductive hormones are found to be essential for cellular activities in brain.

Hypoxia-inducible factors as neuroprotective agent in Alzheimer's disease.

Beta amyloid (Aβ)-42 peptide and phosphorylated tau protein have been demonstrated as the pathological hallmarks of Alzheimer's disease (AD). A gradual decline of oxygen and glucose supply to the brain during aging or hypoxia was manifested as a contributing factor to hypometabolism. The brain regions susceptible to hypometabolism are the hippocampus, entorhinal cortex and cognition-associated neocortical regions like parietal, temporal and frontal cortex.

Structural preferences of Aβ fragments in different micellar environments.

Amyloid diseases occur due to conformational change in the native protein. Understanding the amyloid peptide structural stability and conformational preference at the molecular level in membranous environment may lead to advancement in drug design and therapy. The conformational preferences of amyloid peptide fragments, Aβ₁₋₁₁, Aβ₁₂₋₂₂, Aβ₂₃₋₃₃ and Aβ₃₄₋₄₂ was studied in buffers, trifluoroethanol (TFE) and sodium dodecyl sulfate (SDS) micelles using circular dichroism spectroscopy.

The neuroprotective role of melatonin against amyloid beta peptide injected mice.

Widespread cerebral deposition of a 40-42 amino acid peptide called amyloid beta peptide (A beta) in the form of amyloid fibrils is one of the most prominent neuropathologic features of Alzheimer's disease (AD). The clinical study provides evidence that accumulation of protofibrils due to the Arctic mutation (E22G) causes early AD onset. Melatonin showed beneficial effects in an AD mouse model.

Melatonin prevents amyloid protofibrillar induced oxidative imbalance and biogenic amine catabolism.

Oxidative stress is one of the hypothesized pathogenic mechanisms for neurodegenerative diseases, including Alzheimer's disease (AD); numerous studies suggest that Abeta is toxic to neurons by free radical mediated mechanism. A constant feature in AD brain is selective neuronal loss, accompanied by dysfunction of several neurotransmitter systems, such as cholinergic, serotoninergic and noradrenergic systems. In the present study, we studied the neuroprotective role of melatonin against amyloid protofibrils and the toxicity of protofibrils on serotoninergic and noradrenergic systems.

Inhibitory effects of short-term administration of DL-alpha-lipoic acid on oxidative vulnerability induced by Abeta amyloid fibrils (25-35) in mice.

Abeta amyloid peptide is believed to induce oxidative stress leading to inflammation, which is postulated to play a significant role in the toxicity of Alzheimer's disease (AD). This study was designed to investigate the inhibitory effects of DL-alpha lipoic acid (LA), a potential free radical scavenger, on oxidative vulnerability induced by intraperitoneal injection of Abeta25-35 amyloid fibrils in mice. Mice were divided into three groups: control, Abeta amyloid toxicity induced (AT), and LA treated (ATL).

Association of carnitine deficiency in Indian continuous ambulatory peritoneal dialysis patients with anemia, erythropoietin use, residual renal function, and diabetes mellitus.

Objective: In the present study, we aimed to determine levels of free carnitine in hemodialysis (HD) and peritoneal dialysis (PD) patients in India and to correlate carnitine deficiency with various clinical parameters.

Methods: Patients on HD and PD at two tertiary care centers were selected for the study. Baseline data were obtained, and a free carnitine analysis was performed.

Anti-inflammatory effect of melatonin on A beta vaccination in mice.

A beta vaccination as a therapeutic intervention of Alzheimer's has many challenges, key among them is the regulation of inflammatory processes concomitant with excessive generation of free radicals seen during such interventions. Here we report the beneficial effects of melatonin on inflammation associated with A beta vaccination in the central and peripheral nervous system of mice. Mice were divided into three groups (n=8 in each): control, inflammation (IA), and melatonin-treated (IAM).