Novel therapeutics for Alzheimer's disease: an update.
As the most prevalent form of dementia worldwide, Alzheimer's disease (AD) continues to be a burden for patients and their families. In addition, with the global population of aged individuals increasing exponentially, AD represents a significant economic burden to society. The development of an effective approach for the treatment of AD is thus of major importance, as current treatment strategies are limited to agents that attenuate disease symptomatology without addressing the causes of disease. A considerable need exists for the development of an effective therapy to prevent, or at least delay, the progression of AD. Current hypotheses for the pathogenesis of AD are discussed in this review, with a particular emphasis on the implications of these hypotheses with respect to treatment strategies and preventive measures.
Bonda
David J
DJ
Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA. mark.smith@case.edu
Lee
Hyun-Pil
HP
Lee
Hyoung-gon
HG
Friedlich
Avi L
AL
Perry
George
G
Zhu
Xiongwei
X
Smith
Mark A
MA
D000544:Alzheimer Disease / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control*; D016229:Amyloid beta-Peptides / Q000276:immunology; D000818:Animals; D000906:Antibodies / Q000627:therapeutic use; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007986:Luteinizing Hormone / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects; D016875:tau Proteins / Q000037:antagonists & inhibitors / Q000187:drug effects
D016229:Amyloid beta-Peptides; D000906:Antibodies; D000975:Antioxidants; D004791:Enzyme Inhibitors; D016875:tau Proteins; D018698:Glutamic Acid; D007986:Luteinizing Hormone