Alzheimer’s Disease (AD) ....................................................................................... 72 Cholinergic Decit in AD ........................................................................................ 72 Current Treatment Strategies for AD Are Purely Symptomatic ............................... 73 LA: A Multimodal Drug for the Treatment of AD ................................................... 73

Possible Modes of Action of LA Interfering with AD-Specic Degeneration .... 73 LA: An Activator of ChAT .................................................................................. 73 LA: A Potent Metal Chelator .............................................................................. 74 LA: An Anti-Inammatory Antioxidant and Modulator of Redox-Sensitive Signaling .............................................................................. 74 LA: A Carbonyl Scavenger ................................................................................. 75 LA: A Stimulator of Glucose Uptake and Utilization (“Insulinomimetic”) ....... 75 Upregulation of Glutathione Synthesis via Activation of NRF-2 ....................... 76

Neuroprotective Effects of LA In Vitro and In Vivo ................................................ 78 Protection of Cultured Neurons against Toxicity of Aβ, Iron, and Other Neurotoxins by LA ............................................................................. 78 Protective Effects of LA against Age-Related Cognitive Decits in Aging Rodents ................................................................................... 78 Protective Effects of LA in Rodent Models of AD ............................................. 79

Clinical Trials with LA in AD Patients .................................................................... 79 Combination Treatment of LA with Nutraceuticals ................................................. 81 Acknowledgments .................................................................................................... 83 References ................................................................................................................ 83

Alzheimer’s disease (AD) is a progressive neurodegenerative brain disorder that gradually destroys a patient’s memory and ability to learn, make judgments, communicate effectively, and perform day-to-day tasks. The short-term memory is affected rst, caused by neuronal dysfunction and degeneration in the hippocampus and amygdala. As the disease progresses further, neurons also degenerate and die in other cortical regions of the brain (Stuchbury and Münch, 2005). Sufferers then often experience dramatic changes in personality and behavior, such as anxiety, paranoia, or agitation, as well as delusions or hallucinations (Cummings, 2004). The prevalence of AD in the age bracket of 65-69 years is 1%; 70-74 years, 3%; 75-79 years, 6%; 80-84 years, 12%, and for people aged 85 and over the prevalence is 25%.