Neurotrophic Factors In Brain Research Articles

Growth of Triple Negative and Progesterone Positive Breast Cancer Causes Oxidative Stress and Down-Regulates Neuroprotective Transcription Factor NPAS4 and NPAS4-Regulated Genes in Hippocampal Tissues of TumorGraft Mice-an Aging Connection.

While the refinement of existing and the development of new chemotherapeutic regimens has significantly improved cancer treatment outcomes and patient survival, chemotherapy still causes many persistent side effects. Central nervous system (CNS) toxicity is of particular concern, as cancer patients experience significant deficits in memory, learning, cognition, and decision-making. These chemotherapy-induced cognitive changes are termed chemo brain, and manifest in more than half of cancer survivors. Moreover, recent studies have emerged suggesting that neurocognitive deficits manifest prior to cancer diagnosis and treatment, and thus may be associated with tumor presence, a phenomenon recently termed “tumor brain.” To dissect the molecular mechanisms of tumor brain, we used TumorGraftTM models, wherein part of a patient's tumor is grafted into immune-deficient mice. Here, we analyzed molecular changes in the hippocampal tissues of mice carrying triple negative (TNBC) or progesterone receptor positive (PR+BC) xenografts. TNBC growth led to increased oxidative damage, as detected by elevated levels of 4-hydroxy-2-nonenal, a product of lipid peroxidation. Furthermore, the growth of TNBC and PR+BC tumors altered global gene expression in the murine hippocampus and affected multiple pathways implicated in PI3K-Akt and MAPK signaling, as well as other pathways crucial for the proper functioning of hippocampal neurons. TNBC and PR+BC tumor growth also led to a significant decrease in the levels of neuronal transcription factor NPAS4, a regulator that governs the expression of brain-derived neurotrophic factor (BDNF), and several other key brain neurotrophic factors and pro-survival molecules. The decreased expression of ERK1/2, NPAS4, and BDNF are also seen in neurodegenerative conditions and aging, and may constitute an important tumor brain mechanism.

Effects of asenapine and paliperidone on depression, anxiety and analgesy in mice: Alterations in brain neurotrophic factors, neurogenesis and blood enzyme levels

Effects of asenapine and paliperidone on depression, anxiety and analgesy in mice: Alterations in brain neurotrophic factors, neurogenesis and blood enzyme levels

BDNF over-expression induces striatal serotonin fiber sprouting and increases the susceptibility to l-DOPA-induced dyskinesia in 6-OHDA-lesioned rats

In addition to its role in neuronal survival, the brain neurotrophic factor (BDNF) has been shown to influence serotonin transmission and synaptic plasticity, events strongly implicated in the appearance of l-DOPA-induced dyskinesia (LID), a motor complication occurring in parkinsonian patients after long-term treatment with the dopamine precursor.In order to evaluate a possible influence of BDNF in the appearance of LID, 6-OHDA-lesioned rats received a striatal injection of different concentrations of an adeno-associated viral (AAV) vector over-expressing either BDNF or GFP, as control vector. Eight weeks later, animals started to receive a daily treatment with l-DOPA (4–6mg/kg plus benserazide 4–6mg/kg, s.c.) or saline, and dyskinesias, as well as l-DOPA-induced rotations, were evaluated at several time-points. Moreover, molecular changes in striatal D1 receptor-dependent cAMP/PKA and ERK/mTORC signaling pathways, as well as, sprouting of striatal serotonin axons, were measured. Results showed that the AAV-BDNF vector injection induced striatal over-expression of BDNF, as well as striatal and pallidal serotonin axon hyperinnervation. Moreover, rats that over-expressed BDNF were more prone to develop LID and l-DOPA-induced rotations, compared to the GFP-treated control group. Finally, rats that over-expressed BDNF showed increased levels of striatal D1R-dependent signaling phospho-proteins in response to l-DOPA administration. This study suggests that BDNF over-expression, by inducing changes in pre-synaptic serotonin axonal trophism, is able to exacerbate maladaptive responses to l-DOPA administration.

Factors Responsible for Obesity-Related Hypertension.

The major health issue of being overweight or obese relates to the development of hypertension, insulin resistance and diabetic complications. One of the major underlying factors influencing the elevated blood pressure in obesity is increased activity of the sympathetic nerves to particular organs such as the kidney. There is now convincing evidence from animal studies that major signals such as leptin and insulin have a sympathoexcitatory action in the hypothalamus to cause hypertension. Recent studies suggest that this may involve 'neural plasticity' within hypothalamic signalling driven by central actions of leptin mediated via activation of melanocortin receptor signalling and activation of brain neurotrophic factors. This review describes the evidence to support the contribution of the SNS to obesity related hypertension and the major metabolic and adipokine signals.

Swimming exercise prevents behavioural disturbances induced by an intracerebroventricular injection of amyloid-β1-42 peptide through modulation of cytokine/NF-kappaB pathway and indoleamine-2,3-dioxygenase in mouse brain

Emerging evidence indicates that the activation of indoleamine-2,3-dioxygenase (IDO), a first and rate-limiting enzyme in the kynurenine (KYN) pathway, is involved in amyloid-beta (Aβ1-42)-neurotoxicity and Alzheimer’s disease (AD) pathogenesis. Physical exercise has been considered an effective intervention in AD, attenuating or limiting their progression. Nevertheless, the neurobiological mechanisms underlying the neuroprotective effects of exercise have not yet been fully elucidated. In present study, we investigated the protective effect of an 8-week swimming training (ST) exercise on cognitive and non-cognitive functions and its role in modulating biomarkers of KYN pathway, before an intracerebroventricular (i.c.v.) injection of Aβ1-42 (400pmol/animal; 3μl/site) peptide in mice. Our results demonstrated that ST was effective in preventing the following behavioural disturbances caused by Aβ1-42 injection: memory impairment in the object recognition test and depressive/anxiety-like behaviour in the tail suspension test and elevated plus-maze test, respectively. ST abrogated the neuroinflammatory response and neurotrophic deficiency in the prefrontal cortex and hippocampus induced by Aβ1-42. Also, Aβ1-42 increased IDO activity, KYN and tryptophan (TRP) levels and KYN:TRP ratio in the prefrontal cortex and hippocampus − alterations that were blocked by ST. It can be concluded that ST prevented behavioural and neurobiological deficits induced by Aβ1-42, and suggest that these neuroprotective effects are likely to involve the inhibition of inflammation/IDO activation and up-regulation of neurotrophic factors in brain of mice. Thus, it is possible that physical exercise can be used as a non-pharmacological approach to alleviates both cognitive and non-cognitive symptoms of AD.

BDNF pro-peptide: a novel synaptic modulator generated as an N-terminal fragment from the BDNF precursor by proteolytic processing

Most growth factors are initially synthesized as precursors and it was cleaved into bioactive mature domain and pro-domain. However, compared with the expression and function of bioactive mature domain, the biological role of the pro-domain is poorly understood. Unexpectedly, we found that the pro-domain (or pro-peptide) of brain-derived neurotrophic factor (BDNF), which is well-known neurotrophic factor in brain, has a potential ability to facilitate hippocampal long-term depression. Furthermore, a BDNF polymorphism Val66Met, which substitute valine into methionine at 66 amino acid, impacted the biological activity of the BDNF pro-peptide. We lastly discuss the possible roles of BDNF and its pro-peptide in the generation of neural stem cells and progress of ischemia.

Оособенности вызванной активности мозга при анализе изображений эмоциогенного характера у носителей полиморфных вариантов генов BDNF и HTR2A

The article presents the results of the study of induced brain activity in carriers of polymorphic variants of the gene of the brain neurotrophic factor BDNF and the gene of the receptor serotonin HTR2A, obtained in the evaluation of stimulatory images of emotionogenic character. The image database used in the work included 573 images assigned to three groups: neutral, positive, negative. 40 people of both sexes aged 19—22 years were examined. The isolation of DNA from the buccal epithelium cells was carried out by PCR (OOO «BiReT», Moscow, Russia). During the genetic analysis, the following DNA sections were analyzed: Neurotrophic factor of the brain BDNF, Serotonin receptor HTR2A. To register the electroencephalogram and evoked potentials (EP) of the brain, a multichannel electroencephalograph Neurovisor-136 (manufactured by ISS, Russia) was used. The recording was carried out unipolarly according to the «5—5» scheme in 128 leads. As a result of the study, it was found that in persons with a heterozygous Val / Met genotype of the cerebral neurotrophic factor BDNF, a more pronounced emotional response to both positive and negative stimuli was observed. For persons with a homozygous Val / Val genotype, a more detailed treatment of the details of the visual image is characteristic. For persons with a dominant homozygous G / G genotype of the HTR2A serotonin receptor gene, weighted decision-making in stimulus analysis is characteristic. In individuals with recessive homozygous genotype A / A HTR2A, evaluating the visual stimulus as negative requires the use of significantly larger brain resources, compared to the carriers of the dominant allele G.

Resistance Training Alters the Proportion of Skeletal Muscle Fibers but Not Brain Neurotrophic Factors in Young Adult Rats.

Antonio-Santos, J, Ferreira, DJS, Gomes Costa, GL, Matos, RJB, Toscano, AE, Manhães-de-Castro, R, and Leandro, CG. Resistance training alters the proportion of skeletal muscle fibers but not brain neurotrophic factors in young adult rats. J Strength Cond Res 30(12): 3531–3538, 2016—Resistance training (RT) is related to improved muscular strength and power output. Different programs of RT for rats have been developed, but peripheral and central response has not been evaluated directly in the same animal. To test the hypothesis that RT induces central and peripheral adaptations, this study evaluated the effects of a RT on the performance of a weekly maximum overload test, fiber-type typology, and brain neurotrophic factors in young adult rats. Thirty-one male Wistar rats (65 ± 5 days) were divided in 2 groups: nontrained (NT, n = 13) and trained (T, n = 18). Trained group was submitted to a program of RT ladder climbing, gradually added mass, 5 days per week during 8 weeks at 80% of individual maximum overload. This test was weekly performed to adjust the individual load throughout the weeks for both groups. After 48 hours from the last session of exercise, soleus and extensor digital longus (EDL) muscles were removed for myofibrillar ATPase staining analysis. Spinal cord, motor cortex, and cerebellum were removed for RT-PCR analysis of BDNF and insulin-like growth factor-1 (IGF-1) gene expression. In EDL muscle, T animals showed an increase in the proportion of type IIb fibers and a reduction of type IIa fibers. Insulin-like growth factor-1 gene expression was reduced in the cerebellum of T animals (NT: 1.025 ± 0.12; T: 0.57 ± 0.11). Our data showed that 8 weeks of RT were enough to increase maximum overload capacity and the proportion of glycolytic muscle fibers, but there were no associations with the expression of growth neurotrophic factors.

Dynamics of cognitive disorders in patients with type 2 diabetes mellitus under effect of metabolic therapy

The aim of this study was to investigate the efficiency of metabolic therapy in correction of cognitive impairment in patients with type 2 diabetes. We undertook the analysis of results of the treatment of cognitive dysfunction in 80 patients with a diagnosis of type 2 diabetes. All patients received basic hypoglycemic therapy. 32 patients (study group) received in addition to the basal glucose lowering therapy daily intravenous infusion of 10 mlcytoflavindiluted in 200 ml of a 0.9% sodium chloride solution for 10 days, followed by 2 tablets b.i.d. for 25 days.The group of comparison consisted of 29 patients given in addition to the basal glucose-lowering therapy daily intravenous infusion of 24 ml (600 mg) thioctacid diluted in 200 mL of a 0.9% sodium chloride solution for 10 days. Thereafter, they received 1 tablet of thioctacid BV once daily for 30 days. The control group consisted of 19 patients who received basic hypoglycemic therapy without additional metabolic therapy.Inclusion of cytoflavin in the combined treatment of patients with type 2 diabetes ensured a more effective correction of cognitive impairment. There was a statistically significant improvement in optical-spatial activities (p = 0.001), attention (p = 0.001), abstract thinking (p = 0.046), and memory (p<0.001) compared to those in other groups, according to the MOS test. Positive dynamics was expressed as the improvement of the optical-spatial activities by 9,8 ± 10,3%, attention by 13,5 ± 11,8%, abstract thinking by 7,0 ± 8,9%, and memory by 23.0 ± 14 6%. The study of variations of the serum level of brain neurotrophic factor (BDNF) over time during the treatment with metabolic preparations reveal edits statistically significant increase (p = 0.002) in the patients treated with cytoflavin compared with comparison (p = 0.139) and control (p = 0.078) groups. These results suggest the influence of cytoflavin on the processes of neuroplasticity under conditions of hyperglycemia, improvement of cerebral microcirculation and cerebroprotective action of this medication.

Effect of Zhuang Jing Decoction on Learning and Memory Ability in Aging Rats.

With the average life span of humans on the rise, aging in the world has drawn considerable attentions. The monoamine neurotransmitters and neurotrophic factors in brain areas are involved in learning and memory processes and are an essential part of normal synaptic neurotransmission and plasticity. In the present study, the effect of Zhuang Jing Decoction (ZJD) on the learning and memory ability in aging rats was examined in vivo using Morris water maze. Furthermore, the levels of monoamine neurotransmitters and neurotrophic factors in brain were detected by high-performance liquid chromatography with a fluorescence detector and enzyme-linked immunosorbent assay, respectively. These data showed that oral administration with ZJD at the dose of 30 g·kg(-1) exerted an improved effect on learning and memory ability in aging rats. The results revealed that ZJD could effectively adjust the monoamine neurotransmitters and neurotrophic factors, restore the balance of the level of monoamine neurotransmitters and neurotrophic factors in brain, and finally attenuate the degeneration of learning and memory ability. These findings suggested that ZJD might be a potential agent as cognitive-enhancing drug in improving learning and memory ability. It may exert through regulating the levels of monoamine neurotransmitters and neurotrophic factors in brain, which demonstrated that ZJD had certain antiaging effects.

Effects of chronic administration of adipokinetic and hypertrehalosemic hormone on animal behavior, BDNF, and CREB expression in the hippocampus and neurogenesis in mice.

Neurosecretory cells in corpus cardiacum of insects synthesize a set of hormones that are called adipokinetic, hypertrehalosaemic or hyperprolinaemic, depending on insect in question. This study investigated effects of chronic administration of Anax imperator adipokinetic hormone (Ani-AKH), Libellula auripennis adipokinetic hormone (Lia-AKH), and Phormia-Terra hypertrehalosaemic hormone (Pht-HrTH) on depression, anxiety, analgesy, locomotion in forced swimming (FST), elevated plus-maze (EPM), hot plate, and locomotor activity tests. Ani-AKH (1 and 2 mg/kg), Lia-AKH (1 and 2 mg/kg), and Pht-HrTH (1 and 2 mg/kg) had antidepressant effects in forced swimming test. Lia-AKH (2 mg/kg) and Pht-HrTH (1 and 2 mg/kg) had anxiolytic effects when given chronically in elevated plus-maze test. Ani-AKH (1 and 2 mg/kg) and Pht-HrTH (2 mg/kg) had antinociceptive effects in hot plate test in male balb-c mice. Ani-AKH (2 mg/kg), Lia-AKH (1 and 2 mg/kg), and Pht-HrTH had locomotion-enhancing effects in locomotor activity test in male balb-c mice. Drug treatment significantly increased brain-derived neurotrophic factor (BDNF) and cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) gene expression levels compared to control levels. Pht-HrTH and Ani-AKH groups had significantly increased numbers of BrdU-labeled cells, while neurodegeneration was lower in the Pht-HrTH group. Our study showed that AKH/RPCH family peptides may be used in treatment of psychiatric illness such as depression and anxiety, in treatment of pain and in diseases related to locomotion system. AKH/RPCH family peptides increase neurotrophic factors in brain and have potential proliferative and neuroprotective effects in hippocampal neurogenesis and neurodegeneration.

The standardized Lycium chinense fruit extract protects against Alzheimer׳s disease in 3xTg-AD mice

BackgroundAlzheimer׳s disease (AD) is the most common cause of dementia. This disease is a progressive and irreversible brain disorder accompanied with severe learning and memory impairment. This study investigated whether treatment with standardized Lycii Fructus Extract (LFE) would improve the cognitive function and the pathological features of AD in 3xTg-AD mice. Ethnopharmacological relevanceLycii Fructus is a fruit of Lycium chinense Miller and widely distributed in East Asia and has been used traditionally for anti-aging purposes. Materials and methodsThe cognitive function of 3xTg-AD mice was assessed using the Morris water maze test. The levels of the amyloid beta deposits and NeuN in the hippocampus were evaluated with immunohistochemistry. Brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were examined by western blot analysis. ResultsLFE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the target zone during probe tests. In addition, LFE significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expression of BDNF and TrkB in the 3xTg AD mice. ConclusionsThe present study suggests that LFE treatment can be a useful strategy for treating memory impairment induced by several neurodegenerative diseases.

The Rationale for Exercise in the Management of Pain in Parkinson's Disease.

Pain is a distressing non-motor symptom experienced by up to 85% of people with Parkinson’s disease (PD), yet it is often untreated. This pain is likely to be influenced by many factors, including the disease process, PD impairments as well as co-existing musculoskeletal and/or neuropathic pain conditions. Expert opinion recommends that exercise is included as one component of pain management programs; however, the effect of exercise on pain in this population is unclear. This review presents evidence describing the potential influence of exercise on the pain-related pathophysiological processes present in PD. Emerging evidence from both animal and human studies suggests that exercise might contribute to neuroplasticity and neuro-restoration by increasing brain neurotrophic factors, synaptic strength and angiogenesis, as well as stimulating neurogenesis and improving metabolism and the immune response. These changes may be beneficial in improving the central processing of pain. There is also evidence that exercise can activate both the dopaminergic and non-dopaminergic pain inhibitory pathways, suggesting that exercise may help to modulate the experience of pain in PD. Whilst clinical data on the effects of exercise for pain relief in people with PD are scarce, and are urgently needed, preliminary guidelines are presented for exercise prescription for the management of central neuropathic, peripheral neuropathic and musculoskeletal pain in PD.

Effects of palatable cafeteria diet on cognitive and noncognitive behaviors and brain neurotrophins' levels in mice.

The consumption of palatable high-fat and high-sugar foods have increased dramatically over the past years. Overconsumption of calorically dense food contributes to increasing rates of overweight and obesity that are associated with psychiatry disorders, in particular mood and anxiety disorders. This study evaluated the impact of palatable cafeteria diet (CAF) intake on cognitive and noncognitive behaviors, as well as identified factors related to these behaviors through an evaluation of brain neurotrophic factor (BDNF, NGF, and GDNF) levels in hippocampus of mice. Male Swiss mice received two different diets during 13weeks: standard chow (STA) and highly CAF. Posteriorly, forced swimming test (FST), tail suspension test (TST), plus-maze test (PMT), open-field tests (OFT), and object recognition task (ORT) were utilized as behavioral tests. In addition, brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), and nerve growth factor (NGF) neurotrophins' levels were evaluated in hippocampus of mice. The results demonstrated that mice from the CAF group showed a decrease in the immobility time in the FST and TST. Besides, mice in the CAF group spent more time in the open arms of the PMT. No significant differences were observed in the cognitive behaviors, which were evaluated in the OFT and ORT. In addition, the CAF group showed that BDNF and NGF protein levels increased in the hippocampus of mice. In conclusion, our data suggest that the consumption of palatable high-fat and high-sugar foods induces antidepressant- and anxiolytic-like behaviors, which can be related with BDNF and NGF expression increases in hippocampus of mice in the CAF group.

Effect of vanillin inhalation on brain derived neurotrophic factor in depressed model rats

Objective To evaluate the relieving effects of vanillin sinffing on depression-like behaviors in depressed rats and to explore the possible underlying mechanism. Methods Depression animal model established by chronic unpredictable medium intensity stress combined with isolation and destroy the olfactory bulb. The depressed rats were divided randomly into vanillin inhalation group, fluoxetine hydrochloride group, depression model group, olfactory bulbectomy with the vanillin inhalation treatment group and sham-operated group. Nervous behavioral changes had been observed at different time after the administration of 5 weeks. The concentration of brain derived neurotrophic factor(BDNF) in the brain homogenate and the positive expression of BDNF in hippocampus had been also measured. Results Two weeks after the intervention, the immobility time of vanillin group((12.78±7.50)s) was lower than that of the model group((57.33±32.16)s)(P<0.05). The consumption of saccharose in vanillin group((52.88±25.18)g) was higher than that of model group((37.40±19.33)g)(P<0.05). BDNF of the brain homogenate in vanillin group (0.54±0.13) was significantly increased compared with model group (0.36±0.06) (P<0.01). When compared with the OBX group (0.40±0.06), similar result was obtained. Immunohistochemistry and the average density of image analysis revealed that the expression of BNDF of hippocampal CA3 in vanillin group (0.40±0.03)was significantly increased compared with model group (0.25±0.04) and OBX group(0.28±0.03)(P<0.01). Conclusion Vanillin inhalation significantly relieves depression-like behaviors in depression rats .The possible mechanism may increase hippocampal neurogenesis by raising brain derived neurotrophic factor in brain. Key words: Vanillin; Olfactory pathway; Depressive disorder; Brain derived neurotrophic factor

Effects of preconditioning exercise on brain damage and neurotrophic factor expression after focal brain ischemia in rats

Effects of preconditioning exercise on brain damage and neurotrophic factor expression after focal brain ischemia in rats

Alterations in brain neurotrophic and glial factors following early age chronic methylphenidate and cocaine administration

Attention deficit hyperactivity disorder (ADHD) overdiagnosis and a pharmacological attempt to increase cognitive performance, are the major causes for the frequent (ab)use of psychostimulants in non-ADHD individuals. Methylphenidate is a non-addictive psychostimulant, although its mode of action resembles that of cocaine, a well-known addictive and abused drug. Neuronal- and glial-derived growth factors play a major role in the development, maintenance and survival of neurons in the central nervous system. We hypothesized that methylphenidate and cocaine treatment affect the expression of such growth factors. Beginning on postnatal day (PND) 14, male Sprague Dawley rats were treated chronically with either cocaine or methylphenidate. The rats were examined behaviorally and biochemically at several time points (PND 35, 56, 70 and 90). On PND 56, rats treated with cocaine or methylphenidate from PND 14 through PND 35 exhibited increased hippocampal glial-cell derived neurotrophic factor (GDNF) mRNA levels, after 21 withdrawal days, compared to the saline-treated rats. We found a significant association between cocaine and methylphenidate treatments and age progression in the prefrontal protein expression of brain derived neurotrophic factor (BDNF). Neither treatments affected the behavioral parameters, although acute cocaine administration was associated with increased locomotor activity. It is possible that the increased hippocampal GDNF mRNA levels, may be relevant to the reduced rate of drug seeking behavior in ADHD adolescence that were maintained from childhood on methylphenidate. BDNF protein level increase with age, as well as following stimulant treatments at early age may be relevant to the neurobiology and pharmacotherapy of ADHD.

Role of neurotrophic factor alterations in the neurodegenerative process in HIV associated neurocognitive disorders.

Migration of HIV infected cells into the CNS is associated with a spectrum of neurological disorders, ranging from milder forms of HIV-associated neurocognitive disorders (HAND) to HIV-associated dementia (HAD). These neuro-psychiatric syndromes are related to the neurodegenerative pathology triggered by the release of HIV proteins and cytokine/chemokines from monocytes/macrophages into the CNS -a condition known as HIV encephalitis (HIVE). As a result of more effective combined anti-retroviral therapy patients with HIV are living longer and thus the frequency of HAND has increased considerably, resulting in an overlap between the neurodegenerative pathology associated with HIV and that related to aging. In fact, HIV infection is believed to hasten the aging process. The mechanisms through which HIV and aging lead to neurodegeneration include: abnormal calcium flux, excitotoxicity, signaling abnormalities, oxidative stress and autophagy defects. Moreover, recent studies have shown that defects in the processing and transport of neurotrophic factors such as fibroblast growth factors (FGFs), neural growth factor (NGF) and brain-derived growth factor (BDNF) might also play a role. Recent evidence implicates alterations in neurotrophins in the pathogenesis of neurodegeneration associated with HAND in the context of aging. Here, we report FGF overexpression curtails gp120-induced neurotoxicity in a double transgenic mouse model. Furthermore, our data show disparities in brain neurotrophic factor levels may be exacerbated in HIV patients over 50 years of age. In this review, we discuss the most recent findings on neurotrophins and HAND in the context of developing new therapies to combat HIV infection in the aging population.

Chronic caffeine treatment reverses memory impairment and the expression of brain BNDF and TrkB in the PS1/APP double transgenic mouse model of Alzheimer’s disease

The objective of this study was to investigate the effects of varying doses of caffeine on memory impairment and the expression of brain neurotrophic derived factor (BNDF) and TrkB in PS1/APP double transgenic mouse models. PS1/APP double transgenic mice were administered 0.3 ml/day of saline, 1.5 mg/day of caffeine or 0.75 mg/day of caffeine for eight weeks. A water maze test and western blotting were used to determine the memory capability and expression of hippocampal BNDF and TrkB of the mice. The results demonstrated that 0.75 mg/day and 1.5 mg/day doses of caffeine significantly increased memory capability and the expression of hippocampal BDNF and TrkB in PS1/APP mice with a dose-response effect. The results suggested that chronic caffeine treatment may reverse memory impairment in PS1/APP transgenic mice, and BDNF and its receptor TrkB, may be involved in this process.

Effects of icariin on β-amyloid and neurotrophic factors in brain of mitochondrial deficiency model rats

Effects of icariin on β-amyloid and neurotrophic factors in brain of mitochondrial deficiency model rats