Current Alzheimer Research - Volume 3, Issue 2, 2006

Current Alzheimer Research presents the second issue of its third volume, which comprises nine articles from both primary research and review work. These articles report a combination of mechanism-based and clinicallyoriented translational studies that cover a wide range of Alzheimer's disease (AD) research from the cholinergic model; the role of amyloid, tau protein and metals; to oxidative stress. The present issue rep Read More

Rigorous scientific research has identified multiple interactive mechanisms that parallel and are likely causative of the development of Alzheimer's disease (AD). Causative mechanisms include genomics, the creation of amyloid beta (Abeta), factors inhibiting the Abeta removal process, the transformation of Abeta to its toxic forms (various forms of Abeta aggregation), and lastly the oxidative, inflammatory, and other effects Read More

Alzheimer's disease (AD) is an age-related neurodegenerative disorder that is characterized by a progressive loss in memory and deterioration of the higher cognitive functions. The brain of an individual with AD exhibits extracellular senile plaques of aggregated amyloid-beta-peptide (Aβ), intracellular neurofibrillary tangles (NFTs) that consist of hyperphosphorylated tau protein (P-tau) and a profound loss of basal forebrain Read More

One of the main pathological characteristics of Alzheimer's disease is the presence in the brain of the patients of an aberrant structure, the paired helical filaments, composed of hyperphosphorylated tau. The level of tau phosphorylation has been correlated with the capacity for tau aggregation. Thus, the mechanism for tau phosphorylation could be important to clarify those pathological features in Alzheimer's disea Read More

Treating Alzheimer's disease (AD) is one of today's biggest unmet medical needs. The drugs currently available transiently relieve some symptoms but have no significant effects on the progression of the disease. Progress in the past decade suggests that the amyloidogenesis of the inactive monomeric amyloid β peptide (Aβ) into a subset of toxic Aβ polymers is responsible for neurodegeneration in AD. Not all forms of Aβ ag Read More

The amyloid-b (Aβ) peptide has been linked to the pathology of Alzheimer's disease (AD). There is now evidence to support a vasoconstrictive effect of Aβ protein that could be detected in peripheral skin microvasculature. In this study we investigated the ability of acetylcholinesterase (AChE) inhibitors, Donepezil and Rivastigmine, to modulate the vasoconstrictor activity of Aβ25-35 and Aβ1-40. The ability of these drugs to imp Read More

To determine if there are differential treatment effects of second-generation cholinesterase inhibitors over one year, 130 patients (untreated=65, treated=65) meeting NINCDS-ADRDA criteria for mild or moderate probable AD underwent standardized cognitive testing at baseline and 12 months later at a university memory clinic. Patients were followed either prior to or after the availability of treatment and were matched Read More

Objective: To determine whether Apolipoprotein E4 (Apo E4) gene status or ApoE gene dose affect the lipid profile in AD. Background: Links between hypercholesterolemia and AD development continue to grow. Presently, limited information exists about the influence of the Apo E genotype on the lipid profile characteristics in AD. Methods: We examined the lipid profiles (total cholesterol (TC), high-density lipoprotei Read More

BACKGROUND. Mild Cognitive Impairment is a common condition defined as transitional state between normality and dementia of Alzheimer type. Clinically is characterized by subjective and objective memory loss beyond the expected for age and educational level, although a broad range of cognitive inefficiencies may appear, with preservation of daily living activities. Approximately half the patients convert to dementia withi Read More