Modulation of Amyloid-β and Tau in Alzheimer's Disease Plasma Neuronal-Derived Extracellular Vesicles by Cerebrolysin® and Donepezil.

Background: Plasma neuronal-derived extracellular vesicles (NDEV) contain proteins of pathological, diagnostic, and therapeutic relevance.

Objective: We investigated the associations of six plasma NDEV markers with Alzheimer's disease (AD) severity, cognition and functioning, and changes in these biomarkers after Cerebrolysin®, donepezil, and a combination therapy in AD.

Methods: Plasma NDEV levels of Aβ42, total tau, P-T181-tau, P-S393-tau, neurogranin, and REST were determined in: 1) 116 mild to advanced AD patients and in 20 control subjects; 2) 110 AD patients treated with Cerebrolysin®, donepezil, or combination therapy in a randomized clinical trial (RCT).

Three-dimensional fluoroscopic navigation versus fluoroscopy-guided placement of pedicle screws in L4-L5-S1 fixation: single-centre experience of pedicular accuracy and S1 cortical fixation of 810 screws.

Background: Three-dimensional (3D) navigation techniques can theoretically provide higher accuracy rates and increased safety for pedicle screw (PS) placement than traditional fluoroscopy (FL) guided methods. In this study, we compare the pedicular accuracy of 3D isocentric fluoroscopic navigation (3DFL) versus FL guidance in PS L4-L5-S1 fixation and evaluate the differential cortical purchase and safety of fixation of the S1 PS.

Methods: This is a single-centre retrospective study of 810 PSs placed in open L4-L5-S1 fixation between 2012 and 2017 in 39 patients using standard FL and in 96 patients under 3DFL.

Synergistic Increase of Serum BDNF in Alzheimer Patients Treated with Cerebrolysin and Donepezil: Association with Cognitive Improvement in ApoE4 Cases.

Background: Low circulating brain derived neurotrophic factor may promote cognitive deterioration, but the effects of neurotrophic and combination drug therapies on serum brain derived neurotrophic factor were not previously investigated in Alzheimer's disease.

Methods: We evaluated the effects of Cerebrolysin, donepezil, and the combined therapy on brain derived neurotrophic factor serum levels at week 16 (end of Cerebrolysin treatment) and week 28 (endpoint) in mild-to-moderate Alzheimer's disease patients.

Results: Cerebrolysin, but not donepezil, increased serum brain derived neurotrophic factor at week 16, while the combination therapy enhanced it at both week 16 and study endpoint.

Reduced TNF-α and increased IGF-I levels in the serum of Alzheimer's disease patients treated with the neurotrophic agent cerebrolysin.

According to current scientific knowledge, excess tumour necrosis factor-α (TNF-α) and low insulin-like growth factor-I (IGF-I) are pathogenic-risk factors that constitute therapeutic targets for Alzheimer's disease (AD). Changes in serum TNF-α, total and dissociable IGF-I levels were determined by ELISA in 207 AD patients completing a 24-wk, double-blind, placebo-controlled trial to evaluate the effects of the neurotrophic compound Cerebrolysin (Cere: 10, 30 or 60 ml for 12 wk). At week 24, Cere reduced TNF-α and enhanced dissociable IGF-I with respect to placebo in a dose-related manner.

Reductions in qEEG slowing over 1 year and after treatment with Cerebrolysin in patients with moderate-severe traumatic brain injury.

Changes in quantitative EEG (qEEG) recordings over a 1-year period and the effects of Cerebrolysin (Cere) on qEEG slowing and cognitive performance were investigated in postacute moderate-severe traumatic brain injury (TBI) patients. Time-related changes in qEEG activity frequency bands (increases of alpha and beta, and reductions of theta and delta relative power) and in qEEG slowing (reduction of EEG power ratio) were statistically significant in patients with a disease progress of less than 2 years at baseline, but not in those patients having a longer disease progress time. Slowing of qEEG activity was also found to be significantly reduced in TBI patients after 1 month of treatment with Cere and 3 months later.

Serum TNF-alpha levels are increased and correlate negatively with free IGF-I in Alzheimer disease.

Tumor necrosis factor-alpha (TNF-alpha) and insulin-like growth factor-I (IGF-I) have been involved in the pathogenesis of Alzheimer's disease (AD) as neurotoxic and survival factors, respectively. Recent experimental studies suggest that the signalling pathways of TNF-alpha and IGF-I are functionally interrelated. In order to investigate the possible interaction of TNF-alpha and IGF-I in AD and mild cognitive impairment (MCI), the serum levels of total IGF-I, free IGF-I and TNF-alpha were determined in 141 AD patients, 56 MCI cases and 30 controls.