Decreased degrees of brain-derived neurotrophic factor (BDNF) are assumed to play a crucial role in the pathophysiology of moderate neurocognitive disorders (MNCDs). of memory impairment and total MMSE score in MNCD-AD group. Escitalopram treatment in patients with MNCD-AD or ScVMNCD led to an increase of plasma BDNF concentrations and as a result to a decrease of cognitive depressive and stress symptom severity. In conclusion plasma BDNF might be a reliable biomarker for the validation of MNCD-AD diagnosis and treatment efficacy. 1 Introduction Mild neurocognitive disorders (MNCDs) as an intermediate stage between normal cognitive aging and dementias particularly Alzheimer’s disease (AD) have recently become a subject of an increasing scientific interest [1]. This interest arises from the perspective of significant medical and interpersonal WYE-132 value and potential capability to prevent MNCD conversion into different types of dementias (major neurocognitive disorders). The diagnostic construct of MNCD is usually substantially congruent with the previously proposed nosological entity for moderate cognitive impairment (MCI) [2]. It was shown that overlap between MNCD and MCI diagnosis is usually 98.6% [3]. According to recent epidemiological data the overall prevalence of MNCDs among individuals older than 55 is usually 15.7% with WYE-132 single-domain amnestic multiple-domain amnestic and nonamnestic subtype prevalence of 6.4% 3.7% and 5.6% respectively [4]. Amnestic variants share about 65% in the structure of MNCDs [5]. The main etiological type of amnestic MNCDs is usually MNCD due to Alzheimer’s disease (MNCD-AD) [6]. The second common etiological type of MNCD is usually subcortical vascular one (ScVMNCD) with the prevalence of 37.3% [7]. ScVMNCD manifests with clinical symptoms of subcortical vascular dementia though the severity of the impairment does not reach the level of WYE-132 dementia and cognitive deficit does not interfere with the capacity for self-reliance in everyday actions [8]. The analysis of neurobiological areas of MNCDs might reveal some pathogenetic systems that could become goals for administration of MNCDs. The appearance of growth elements specifically brain-derived neurotrophic aspect (BDNF) is normally one of these. In nearly all neurodegenerative and vascular dementias a reduced amount of BDNF focus in the mind and concurrently in plasma [9] or serum continues to be reported [10 11 Furthermore a rise of BDNF appearance has been seen in sufferers acquiring selective serotonin reuptake inhibitors (SSRIs) and antidement medications [10]. Therefore we’re able to suppose that the loss of plasma/serum BDNF level may be used being a natural marker of MNCD’s medical WYE-132 diagnosis whereas the boost of the neurotrophin may be employed for the evaluation of treatment effectiveness. Limited information is definitely available WYE-132 for plasma/serum BDNF concentrations in individuals with MNCDs. Although low levels of BDNF in serum [12] and plasma [13] were found in individuals with MNCD-AD no studies are available concerning BDNF levels in individuals with ScVMNCD so far. Consequently a comparative study of plasma BDNF levels in different etiological types of MNCDs seems to be relevant. The current lack of effective MNCD’s treatment based on a high-level evidence warrants a search for new approaches based on neuroprotective strategies. Hence the purpose of our study was to evaluate plasma BDNF concentrations in individuals with the main etiological types of MNCDs and to determine whether the assessment of plasma BDNF level could improve the diagnostics of MNCD-AD and ScVMNCD. We also targeted to study the dynamics of plasma BDNF in MNCD-AD/ScVMNCD individuals after escitalopram treatment. We selected escitalopram taking into account the evidence about its activation of BDNF manifestation [14] a frequent comorbidity of MNCDs Rabbit polyclonal to AKR1A1. and depressive or/and panic disorders [15] as well as WYE-132 the priorities of escitalopram effectiveness and safety with this medical establishing [16]. 2 Materials and Methods 2.1 Subject matter and Methods 59 individuals over 65 years were enrolled in the study. 21 individuals met the diagnostic criteria for possible MNCD-AD relating to DSM-5 [2]. 22 individuals fulfilled the diagnostic criteria for ScVMNCD relating to Frisoni et al. [8] and probable neuroimaging-supported analysis of vascular MNCD relating to DSM-5 [2]..