The results of the analysis of comparative studies of neurotrophic drugs based on brain hydrolysates (BH) are presented. The most comprehensive comparative study of the BH drugs carried out by Zhang, et al. 2019 investigated the effects of four drugs (cognistar, cerebrolysate, cortexin, cerebrolysin) on a model of ischemic stroke in rats. The study showed that a significant improvement in the neurological outcome compared with placebo was observed only with cerebrolysin. Higher standardization in elemental composition, higher antioxidant activity, and presence of active peptide fragments of neuropeptides of nerve growth factor, enkephalins, orexin and galanin in cerebrolysin explains neurotrophic and neuroprotective effects of the drug.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.17116/jnevro2019119101134 | DOI Listing |
Alzheimers Dement
December 2024
Glenn Biggs Institute for Alzheimer's & Neurodegenerative Diseases, University of Texas Health Science Center, San Antonio, TX, USA.
Background: Disrupted sleep patterns have been shown to exacerbate Alzheimer's disease (AD) risk, potentially because of sleep's role in memory consolidation and synaptic plasticity. Recent evidence highlights that high brain-derived neurotrophic factor (BDNF) levels, a protein enabling neuroplasticity and memory functions, could play a protective role in age related cognitive impairment. We examined the association between total sleep time and cognition, and BDNF levels as a potential modifier.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Laboratory of Clinical Investigation, National Institute on Aging, Intramural Research Program, Baltimore, MD, USA.
Background: The choroid plexus (CP), a vital component in the brain's ventricles, is crucial for cerebrospinal fluid (CSF) production and maintenance of the brain's physiological environment. It plays a key role in regulating neuroinflammatory responses, clearing harmful substances, producing neurotrophic factors and signaling molecules, and forming blood-CSF barrier. Consequently, changes to the CP's structural integrity could disrupt brain homeostasis and lead to cognitive impairment.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Geriatric Research Education and Clinical Center William S. Middleton VA Hospital, Madison, WI, USA.
Background: Brain-derived neurotrophic factor (BDNF)-a key neurotrophin involved in synaptic plasticity, neurogenesis, and neuroprotection-has been shown to mediate sex differences in verbal learning and memory (VLM) ability, but it remains unclear whether this relationship is conditionally dependent upon carriage of the Val66Met polymorphism in the BDNF gene. This study investigates how BDNF carriage influences the mediation of sex differences in VLM scores by plasma BDNF levels in a cohort enriched for AD risk.
Method: Cognitively unimpaired participants in the Wisconsin Registry for Alzheimer's Prevention (WRAP; n=198, age 63.
Background: Older adults with type 2 diabetes (T2D) are more likely to develop Alzheimer's disease (AD) due to impaired brain metabolism. Although the underlying mechanisms of this relationship are largely unknown, lower levels of brain-derived neurotrophic factor (BDNF) -which promotes hippocampal neurogenesis in adulthood- and atrophy of the hippocampus are evident in patients with T2D and dementia, possibly linking the two conditions. The hippocampus is comprised of multiple subfields, each with their respective functions, cellular composition, and age-related sensitivity.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Turner Institute for Brain and Mental Health, School of Psychological Sciences, Monash University, Melbourne, VIC, Australia.
Background: In the presence of abnormally high amyloid (Aβ+), carriage of the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism Met allele (Met66) is associated with faster clinical disease progression, greater neuronal loss and faster rate of CSF total-tau and p-tau compared to matched Val66 Aβ+ homozygotes. Aβ levels are unaffected by carriage of Met66. This suggests reduced neurotrophic support may accelerate Aβ-related neuronal dysfunction and cognitive decline.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!