title: Therapeutic perspectives of drugs targeting Toll-like receptors based on immune physiopathology theory of Alzheimer's disease.
abstract: Alzheimer's disease (AD) is a neurodegenerative disease associated with the development of dementia. It has been established that the pathological hallmarks of neurofibrillary tau protein tangles and senile β-amyloid protein plaques lead to degeneration of neurons via inflammatory pathways. The progressive death of neurons, primarily cholinergic, results in a gradual and fatal decline of cognitive abilities and memory. By targeting these pathological hallmarks and their associated pathways, AD drug therapy can potentially attenuate the disease state. In this review article, we focus on newly proposed and experimental AD drug treatment. We discuss three characteristic areas of AD treatment: prevention of neurotoxic β-amyloid protein plaque formation, stability of neuronal tau proteins, and increase in neuronal growth and function. The primary drug therapy methods and patents discussed include the use of neurotrophic factors and targeting of the amyloid precursor protein cleavage pathway as prevention of β-amyloid formation and tau aggregation.
authors.forename: Andrew R
authors.initials: AR
authors.lastname: Schneider
authors.affiliation: University of Toledo, College of Pharmacy and Pharmaceutical Sciences, Department of Pharmacology, Health Science Campus, 3000 Arlington Avenue, Toledo, OH 43614, USA. youssef.sari@utoledo.edu.
authors.forename: Youssef
authors.initials: Y
authors.lastname: Sari
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D014150:Antipsychotic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D051193:Toll-Like Receptors / Q000378:metabolism*
chemical_list: D016229:Amyloid beta-Peptides; D014150:Antipsychotic Agents; D051193:Toll-Like Receptors