Alzheimer’s disease (AD) is a neurological disorder in which the neuronal degeneration associated with inflammatory processes and oxidative stress. Since alpha-terpineol was shown to possess antioxidant anti-inflammatory effects, administration of this compound studied on rat model AD. To create model, Aβ1-42 injected into hippocampus male Wistar rats. Generated AD models were divided simple sh...

Objective(s): Amyloid β plaques, in Alzheimer’s disease, are deposits in different areas of the brain such as prefrontal cortex, molecular layer of the cerebellum, and the hippocampal formation. Amyloid β aggregates lead to the release of cytochrome c and finally neuronal cell death in brain tissue. hCG has critical roles in brain development, neuron differentiation, and function. Therefore, we...

BACKGROUND Understanding the mechanisms of amyloid-beta protein (Abeta) production and clearance in the brain has been essential to elucidating the etiology of Alzheimer disease (AD). Chronically decreasing brain Abeta levels is an emerging therapeutic approach for AD, but no such disease-modifying agents have achieved clinical validation. Certain proteases are responsible for the catabolism of...

Human apolipoprotein (ApoE) genotype influences the development of Alzheimer's disease and cerebral amyloid angiopathy (CAA). Specific mutations within the amyloid-beta protein (Abeta) peptide have been identified that cause familial forms of CAA. However, the effect of APOE genotype on accumulation of CAA mutant Abeta in brain is not well understood. In the present study, we determined how hum...

Up to the present, Alzheimer’s disease (AD), a dementia, is believed to be incurable; even its cause has not been documented. A few hypotheses have been postulated, however; among these are the destruction of acetylcholine by the enzyme acetylcholineesterase, the accumulation of amyloid beta plaque, and peroxidation of the brain cells. Since the disease was unknown in the olden days in Thailand...

Wolfson Drug Discovery Unit, Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, Royal Free Campus, University College London, Rowland Hill Street, London NW3 2PF, UK Division of Neuropathology and Department of Neurodegenerative Disease, and Stroke Research Group, Department of Brain Repair and Rehabilitation, Institute of Neurology, University College London, Queen Square, ...

Cerebral accumulation of amyloid-beta (Abeta) is characteristic of Alzheimer disease and of amyloid precursor protein (APP) transgenic mice. Here, we assessed the efficacy of CI-1011, an inhibitor of acyl-coenzyme A:cholesterol acyltransferase, which is suitable for clinical use, in reducing amyloid pathology in both young (6.5 months old) and aged (16 months old) human APP transgenic mice. Tre...

A monoclonal antibody (YK-2), which was previously established to react with apolipoprotein E (apoE) peptides in systemic amyloid deposits, was further characterized. Epitope of this antibody was determined to be the residue 221 to 230 of apoE. In comparison with polyclonal anti-apoE antibodies, this antibody showed strong reactivity with apoE peptides in amyloid fibril preparation but poor rea...

Here we present the ascidian Ciona intestinalis as an alternative invertebrate system to study Alzheimer's disease (AD) pathogenesis. Through the use of AD animal models, researchers often attempt to reproduce various aspects of the disease, particularly the coordinated processing of the amyloid precursor protein (APP) by alpha-, beta- and gamma-secretases to generate amyloid beta (Abeta)-conta...

The characteristic neuropathological changes associated with Alzheimer's disease (AD) and other lines of evidence support the amyloid cascade hypothesis. Viewing amyloid deposits as the prime instigator of dementia has now led to clinical trials of multiple strategies to remove or prevent their formation. We performed neuropathological and biochemical assessments of 3 subjects treated with bapi...