Current Pharmaceutical Design - Volume 12, Issue 33, 2006

Alzheimer's disease (AD), one of the current major health problems, is already approaching epidemic proportions, affecting millions of people worldwide, while an effective curative or preventive therapy still remains elusive. Ever since the discovery of the direct relationship between most cholinergic markers in the central nervous system and the cognitive and functional decline experienced by AD patients, as well as the su Read More

Alzheimer's disease (AD) is the most common cause of age-related cognitive decline. Both active and passive immunization paradigms have illustrated the potential to prevent and reverse established AD pathology in transgenic and non-transgenic animal models of AD. Follow-up studies have shown that changes in amyloid burden observed with immunization could rescue cognitive deficits in both young and aged mice. D Read More

Alzheimer's disease is a form of sporadic, age-related dementia. According to the “amyloid hypothesis”, the processing of β-amyloid precursor protein (APP) leads to the formation of senile plaque aggregates which subsequently congest normal neurological functions. Currently, prophylaxis is testimonial, while treatment relies mainly on symptomatic relief. This review emphasizes the importance of disrupting the pathological Read More

Alzheimer disease (AD) is characterized by excessive deposition of amyloid β-peptides (Aβ peptides) in the form of senile plaques as well as neurofibrillary tangles (NFTs) in the brain. In the amyloidogenic pathway, the amyloid-β precursor protein (APP) is cleaved by β-secretase first, followed by γ-secretase cleavage producing therefore Aβ. This review summarizes the recent findings in the AD field and focuses on the Read More

The amyloid-β (Aβ) peptides and in particular the longer, highly amyloidogenic isoform Aβ42 are believed by many to be the central disease-causing agents in Alzheimer's disease (AD). Consequently, academic and pharmaceutical laboratories have focused on elucidating the mechanisms of Aβ production and developing strategies to diminish Aβ formation for treatment or prevention of AD. The most substantial advances Read More

Neuritic plaques composed mainly of amyloid β-protein (Aβ) in the brain are an early and invariant neuropathological feature of Alzheimer's disease (AD). The current search for anti-AD drugs is mainly focused on modification of the process of Aβ deposition in the brain. In this article, the recent development of the molecules that inhibit the formation of β-amyloid fibrils (fAβ), as well as destabilize preformed fAβ is reviewed. Rece Read More

Although the hallmarks of neurodegeneration in Alzheimer's brains are well known, one of the current difficulties is related to the lack of solid evidence about the ultimate factors that give rise to the pathogenesis of this disease, creating a great challenge for the definition of efficient treatments for Alzheimer's disease (AD). Current therapeutic option for AD patients is the use of acetylcholinesterase (AChE) inhibitors, Read More

The purpose of this review is to discuss the pathophysiological pathways involved in pathogenesis of Alzheimer's disease pointing out current and future pharmacological targets. Alzheimer's disease is one of the most important neurodegenerative disorders in the developed world together with Parkinson's disease. Although this disease was described almost a century ago, the molecular mechanisms that lead to the develop Read More