%0 Journal Article
%T Biomarkers in Alzheimer's Disease: A Review
%A Meena Chintamaneni
%A Manju Bhaskar
%J ISRN Pharmacology
%D 2012
%R 10.5402/2012/984786
%X Alzheimer's disease is the most common form of dementia affecting millions of individuals worldwide. It is currently diagnosed only via clinical assessments and confirmed by postmortem brain pathology. The development of validated biomarkers for Alzheimer's disease is essential to improve diagnosis and accelerate the development of new therapies. Biochemical and neuroimaging markers could facilitate diagnosis, predict AD progression from a pre-AD state of mild cognitive impairment (MCI), and be used to monitor efficacies of disease-modifying therapies. Cerebrospinal fluid (CSF) levels of A¦Â40, A¦Â42, total tau, and phosphorylated tau have diagnostic values in AD. Measurements of the above CSF markers in combination are useful in predicting the risk of progression from MCI to AD. New potential biomarkers are emerging, and CSF or plasma marker profiles may eventually become part of the clinician's toolkit for accurate AD diagnosis and management. These biomarkers along with clinical assessment, neuropsychological testing, and neuroimaging could achieve a much higher diagnostic accuracy for AD and related disorders in the future. 1. Background Alzheimer¡¯s disease (AD) is a neurological disorder and is the most prevalent form of age-related dementia in the modern society [1]. With increasing life expectancy, dementia is a growing socioeconomic and medical problem. Many factors have been linked to the incidence of AD, including age, gender (females are more likely to be affected), genetic factors, head injury, and Down¡¯s syndrome. It is estimated that, by 2050, the number of people aged 80 years or older will approach 370 million worldwide and that 50 percent of those aged 85 years or older will be afflicted with AD [2]. The diagnosis of AD is made by postmortem analysis of brains of patients with dementia. Intracellular neurofibrillary tangles (NFT) containing hyperphosphorylated tau protein and apolipoprotein E and extracellular senile (neuritic) plaques containing many proteins, including ¦Â-amyloid (A¦Â), ¦Á-synuclein, ubiquitin, apolipoprotein E, presenilins, and alpha antichymotrypsin, are considered pathological hallmarks of AD. Lewy bodies are present in the brains of about 60% of AD cases [3]. The pathogenic process of AD probably starts decades before clinical onset of the disease. During this preclinical period, there is a gradual neuronal loss. The first symptoms, most often impaired episodic memory, appear at a certain threshold. This clinical phase is often designated as mild cognitive impairment (MCI) [4]. To date, a definitive diagnosis of AD can
%U http://www.hindawi.com/journals/isrn.pharmacology/2012/984786/