Traditional used Plants against Cognitive Decline and Alzheimer Disease

Gunter Peter Eckert

doi:10.3389/fphar.2010.00138

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by progressive memory deficits, impaired cognitive function, and altered and inappropriate behavior. Aging represents the most important risk factor for AD and the global trend in the phenomenon of population aging has dramatic consequences for public health, healthcare financing, and delivery systems in the word and, especially in developing countries. Mounting evidence obtained in in vitro and in vivo studies, suggests that various traditionally used plants in Asia, India, and Europe significantly affect key metabolic alterations culminating in AD-typical neurodegeneration. The present article aims to bring the reader up-to-date on the most recent studies and advances describing the direct and indirect activities of traditional used plants and its constituents possibly relieving features of AD. A variety of traditional used plants and its extracts exerted activities on AD related drug targets including AChE activity, antioxidative activity, modulation of Aβ-producing secretase activities, Aβ-degradation, heavy metal chelating, induction of neurotrophic factors, and cell death mechanisms. Although pre-clinical investigations identified promising drug candidates for AD, clinical evidences are still pending.

Highlights

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized clinically by progressive memory deficits, impaired cognitive function, and altered and inappropriate behavior (Mattson, 2004)
AD is considered as a protein aggregation disorder, based on two key neuropathological hallmarks, namely the hyperphosphorylation of the tau protein resulting in the formation of neurofibrillary tangles (NFTs), and the increased formation and aggregation of amyloid-beta peptide (Aβ) derived from amyloid precursor protein (APP) (Haass and Selkoe, 2007)
Results indicated that DSS ameliorates age-related memory dysfunction, modulates metabolism of monoamine neurotransmitters, and protects ultra structure of the cortex (Kou et al, 2005). These findings suggest that DSS may be a useful therapeutic agent for senile dementia, especially AD (Kou et al, 2005)

Summary

Introduction

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized clinically by progressive memory deficits, impaired cognitive function, and altered and inappropriate behavior (Mattson, 2004). AD represents the most common form of dementia, which places a considerable and increasing burden on patients, caregivers, and society. Brain regions involved in learning and memory processes, including the temporal and frontal lobes as well as the hippocampus, are reduced in size in AD patients as the result of degeneration of synapses and death of neurons (Arendt, 2009). AD is considered as a protein aggregation disorder, based on two key neuropathological hallmarks, namely the hyperphosphorylation of the tau protein resulting in the formation of neurofibrillary tangles (NFTs), and the increased formation and aggregation of amyloid-beta peptide (Aβ) derived from amyloid precursor protein (APP) (Haass and Selkoe, 2007). The exact underlying cause initiating the onset of AD is still unclear, an imbalance in oxidative and nitrosative stress, intimately linked to mitochondrial dysfunction, characterizes already early stages of AD pathology (Müller et al, 2010)

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