The diagnostic evaluation of patients suspected of having AD comprises (i) a history from a reliable informant (containing general medical history, neurological history, neuropsychiatrie history, family history); (ii) physical and neurological examination; (iii) routine laboratory examinations (complete blood count, sequential multiple analysis-21 , thyroid function tests, vitamin B12, folate,

rapid plasma reagin); optional laboratory examinations (erythrocyte sedimentation rate, human immunodeficiency virus (HIV) serology, serology Inhibitors,research,lifescience,medical for Lyme’s disease, urinalysis, urine drug screen, lumbar puncture, electroencephalography); and (iv) neuroimaging (computed tomography Inhibitors,research,lifescience,medical or magnetic resonance imaging). Neuropathological examination (looking for the hallmark senile plaques and neurofibrillary tangles) from autopsy studies suggest a 90% accuracy rate in the clinical detection of AD – if it is done by using standardized criteria such as those of the Diagnostic and Statistical Manual of Mental Disorders, 4th Tipifarnib CAS edition (DSM TV) criteria1 (Table I) and the National Institute of Neurological and Communicative Diseases and Stroke – Alzheimer’s Disease and Related Disorders Association (NINCDS-ADRDA) criteria (Table II).2 Table I Diagnostic criteria for Dementia of the Alzheimer’s

Type (DSM-IV). Reproduced from ref 1: selleck chem inhibitor American Psychiatric Association. Diagnostic Inhibitors,research,lifescience,medical and Statistical Manual of Mental Disorders. 4th ed. Washington,

DC; 1994. Copyright © 1994, American Psychiatric … Table II National Institute of Neurological Inhibitors,research,lifescience,medical and Communicative Diseases and Stroke – Alzheimer Disease and Related Disorders Association (NINCDS-ADRDA) criteria for diagnosis of Alzheimer’s dementia. The course of AD tends to be slowly progressive, with a loss of 3 to 4 points per year on a standard assessment instrument Inhibitors,research,lifescience,medical such as the Mini-Mental State Examination (MMSE). Various patterns of deficit are seen, with the most common being an insidious onset, with recent memory loss followed by the development of aphasia, apraxia, and agnosia after several years. Some patients present with irritability and personality changes in the Brefeldin_A early stages. In the later stages, patients usually develop gait and motor disturbances, eventually becoming mute and bedridden. On average, AD patients live for 8 to 10 years after they are diagnosed, although the disease can last for up to 20 years.3 Comorbidity Although still the most common form of dementia, AD can be comorbid with Lewy-body dementia or vascular dementia. There are limited clinical data in treating patients with this type of comorbidity. Patients with AD also have a high degree of medical comorbidity (heart disease, diabetes, cancers). Etiology The main neuropathological features of AD appear to be senile plaques and neurofibrillary tangles.