We thus postulate that AD patients with svCVD (mixed ML323 supplier AD) will demonstrate greater cognitive benefit with cognitive enhancers. In this study, we compared the effectiveness of cognitive enhancers

between AD patients with and without svCVD in a real-world tertiary clinic setting. 2 Methods 2.1 Study Design and Study Sample The study was a retrospective review of a prospective electronic clinical database of dementia patients with data on diagnosis, treatment, follow-up (monitoring), and cognitive and functional outcomes. The study was approved by the Institutional Review Board. The study sample included outpatients from a tertiary dementia clinic, who were enrolled between January 2006 and July 2013. Sociodemographic, clinical (including use of cognitive enhancers), and outcome information on these patients were recorded on our medical electronic database. We focused primarily on cognitive outcomes, and considered the cognitive enhancers acetylcholinesterase inhibitors and N-methyl-d aspartate (NMDA) antagonists. We queried the database for all dementia outpatients who satisfied the selleck products following inclusion criteria: diagnosis of mild to moderate AD based on Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision (DSM-IV TR) criteria [19], clinical dementia rating (CDR) of 1–2 [20],

availability of neuroimaging https://www.selleckchem.com/products/17-DMAG,Hydrochloride-Salt.html data and Mini-Mental State Examination (MMSE) score [21], and treatment with cognitive enhancers for at least 6 months. Patients who had a break in the use of cognitive enhancers for more than 3 months were excluded from the study. Of 951 dementia

patients seen from January 2006 to July 2013, a total of 165 eligible patients were identified. Of these, 137 (83 %) patients had mixed AD (AD + svCVD) and 28 (17 %) patients had AD without svCVD (pure AD) (Fig. 1). Fig. 1 Flow diagram of eligible patient selection. MMSE Mini-Mental State Examination, MRI magnetic resonance imaging 2.2 Measurements AD was diagnosed based on Carnitine palmitoyltransferase II the DSM-IV TR criteria. The presence of WMH on brain magnetic resonance imaging (MRI) was used as a surrogate marker for svCVD. WMH were semi-quantitatively rated using the modified-Fazekas scale on T2-weighted MRI images by an experienced clinician [22]. Periventricular WMH (pv-WMH) was graded as 0 = absence, 1 = ‘caps’ or thin lining, 2 = ‘halo’, and 3 = irregular pv-WMH extending into the white matter. Deep subcortical WMH (dsc-WMH) was rated as 0 = absence, 1 = punctuate foci, 2 = confluent foci and 3 = large confluent areas. Total score was obtained by the summation of pv-WMH and dsc-WMH in the right and left hemispheres for a total score of 12. AD patients with a total WMH score of ≥6 points were classified as mixed AD, and pure AD otherwise.