Current Alzheimer Research - Volume 1, Issue 3, 2004

Alzheimer's disease (AD) respects not privilege, rank, nor fame. It is among the great equalizers that strike where they will and reveal the fundamental human unity we all share. In November of 1994, the world was shown this when Ronald Reagan, 40th president of the United States of America, announced that he had been diagnosed as a likely case of AD [1]. As of June of 2004, his long struggle has ended. He announc Read More

Site-directed antibodies which modulate conformation of β-amyloid peptide became the theoretical basis of the immunological approach for treatment of Alzheimer's disease (AD). Indeed, antibodies towards the EFRH sequence, located between amino acids 3-6 of the N-terminal region of Alzheimer's AβP, found to be a key position in protein conformation modulation, suppress formation of β-amyloid and dissolve already fo Read More

Alzheimer's disease, as well as most of other neurodegenerative disorders, is characterized by the deposition of insoluble proteinaceous aggregates. Hence, any intervention aimed at reducing this process could be envisioned as a therapeutic way to slow down the disease. In the case of Alzheimer's disease, the culprit protein is the 40-43 amino acidlong amyloid b peptide (Aβ). This fragment is generated from the β-am Read More

Accumulation of the amyloid β-peptide (Aβ) in the brain is believed to initiate a series of neurotoxic events that causes neurodegeneration in Alzheimer´s disease (AD). Aβ is generated by processing of the β-amyloid precursor protein (APP) through the successive action of two proteolytic enzymes, β-secretase and γ-secretase. While β-secretase has been identified as the membrane-bound aspartyl protease BACE, the iden Read More

Fibrillar amyloid beta-protein (Aβ) is the principal component of amyloid plaques in the brains of patients with Alzheimer's disease. We have studied the effect of walnut extract on Aß fibrillization by Thioflavin T fluorescence spectroscopy and electron microscopy. The walnut extract not only inhibited Aß fibril formation in a concentration and time- dependent manner but it was also able to defibrillize Aβ preformed fibrils. Over Read More

The cholinergic hypothesis of Alzheimer's Disease (AD) has led to a number of animal models to study in vivo the pathogeny of cortical cholinergic involution. The lesion of the cholinergic neurons of the basal forebrain, especially of the nucleus basalis magnocellularis (nbm) of rodents, has been the most utilized method for obtaining these models. Toxic substances such as quinolic, kainic, NMDA, ibotenic and quisqualic acids, the Read More

Genetic factors are involved in the aetiology of dementias. Three genes have been identified which, when mutated, cause Familial Alzheimer disease (FAD): the presenilin-1 (PS1), the presenilin-2 (PS2) and the amyloid precursor protein (APP) genes. Together, these mutations are responsible for 30-50% of the cases with autosomal dominant Alzheimer disease (AD), and for about 5% of all AD cases. While over 130 Read More

Dementia, Alzheimer's disease (AD) being the most common cause of it, is a major and growing medical and social problem, particularly in the advanced age, with the highest rate in the population over 75 y. Recent sophisticated therapeutic measures require more sensitive diagnostic tests to recognize early stages of the disease. In this paper, the current neuronuclear imaging literature is reviewed with regard to early and Read More