To counteract the death of DN, Salehi and Mashayekhi [ 31 ] proposed that BDNF is produced by glial cells that increase their population as a result of an active response to neurodegeneration, since they reported an increase in BDNF levels in cerebrospinal fluid of patients with PD [ 31 ].
In addition, miR-1 levels have been found to be decreased in patients with PD compared with healthy individuals [ 36 ]. Zhang et al. To corroborate the results, they performed the inhibition of miRp and observed that the levels of BDNF increased and the survival of the tyrosine hydroxylase-positive DN of the SN in mice injected with MPTP was also significantly improved.
Another factor that alters the secretion of BDNF is the single nucleotide functional polymorphism Val66Met, whose effect has been widely studied in humans [ 39 , 40 , 41 ]. This polymorphism consists of a substitution of valine amino acid by methionine at position 66 of the precursor protein pro-BDNF causing a decrease in secretion induced by depolarization [ 42 ]. Recently, it was found that this protein interacts with the neurotrophic receptor TrkB, inhibiting its internalization and its correct distribution.
The inhibition of this neurotrophic factor makes them susceptible to the DN of the SN and contributes to the symptoms observed in PD. The degenerative process develops mainly in the DN. In humans, the early loss of dopaminergic neurons from the SN drastically reduces the striatal dopamine concentration [ 53 , 54 ]. The origin of the motor and non-motor alterations can be sporadic due to genetic deregulation. Independent of the etiologic origin, patients with PD develop motor and even cognitive dysfunctions.
The bradykinesia or slowness of movement is manifested by the decrease in manual dexterity or the difficulty to get up from where they are sitting. Also during the progress of the disease, patients show postural instability with increased risk of falls as they take much faster and shorter steps, and postural instability has a poor response to dopamine treatments [ 58 ].
The symptoms of PD are progressive; however, the rate of progression in motor symptoms is variable according to the period of development of the disease in which they occur [ 60 ]. In functional magnetic resonance imaging studies fMRI of akinetic patients, changes have been observed during the performance of a complex sequential motor task, showing a reduced functional magnetic resonance signal in the rostral part of the supplementary motor area and in the right dorsolateral prefrontal cortex.
In addition, these patients also showed a significant bilateral increase in the activation of the primary sensorimotor cortex, the premotor cortex lateral, the caudal part of the supplementary motor area, the inferior parietal cortex and the anterior cingulate cortex, and in other cortical motor areas [ 61 ]. It has been mentioned that during the earliest pathological stage of PD, neuronal degeneration occurs in motor nuclei of the brainstem, olfactory bulbs and limbic areas; as it proceeds, it continues to the temporal and paralimbic cortices, as well as to the thalamic nuclei, until reaching associative areas such as the prefrontal lobes, and to finally involve the first order and sensory motor areas [ 62 , 63 , 64 ].
However, Agosta et al. They also observed that a microstructural damage of the white matter WM occurs with the increase in the severity of the disease, involving the brainstem, cerebellum, thalamocortical, interhemispheric and limbic pathways, as well as the extra motor association tracts.
They correlate the damage in WM with the degree of cognitive deficit, considering that the damage in WM probably contributes to the more severe motor and non-motor dysfunctions that occur in patients in later stages. In addition, alterations in visuospatial, attentional, executive and memory functions may occur [ 66 ]. The incidence of dementia is approximately per , patients per year among patients with PD, suggesting that people with PD have a three to six times greater risk of developing dementia than people of the same age without PD [ 68 ].
However, the pathophysiological mechanisms involved in these cognitive deficits are not yet clear. At present, neurotrophic factors have attracted attention from both clinical and experimental levels. BDNF is one of the key molecules in the modulation of cerebral plasticity and can induce long-term potentiation LTP through the activation of signal transduction routes; this LTP plays a key role in the neurophysiological basis for learning and memory [ 69 ].
In experimental animal models, it has been observed that the inhibition of BDNF signaling in knockout mice can affect spatial learning and memory; on the contrary, in the general population, it has been observed that at higher levels of BDNF in the hypothalamus there is a better cognitive function, including memory [ 70 ].
At the clinical level, there has been an association between serum BDNF levels and cognitive impairment. For example, one study observed the association between the decreased levels of BDNF present in cerebrospinal fluid, which contributes to early cognitive deterioration in PD, in particular to executive-attentional dysfunction [ 20 ]. On the other hand, an increase in BDNF concentrations has been detected in the same sample type of individuals with this pathology with respect to non-diseased controls [ 31 ], which could be due to a glial activation to increase the synthesis of this neurotrophin in response to brain damage [ 19 ].
Schematic representation showing the structure and location of BDNF gene and the location of single nucleotide polymorphism SNP that leads to the disease. BDNF, brain-derived neurotrophic factor. The hippocampus is an important nucleus for learning and memory consolidation processes, and since BDNF plays an important role in the neuroplasticity of the hippocampus, the absence of this neurotrophin might affect the processes of learning and memory in the short and long term.
In studies of patients with dopaminergic neurodegeneration, a reduction in serum BDNF levels was observed, accompanied by a loss of striatal dopamine transporter DAT binding, that is, a positive correlation was found between the striatal DAT junction and BDNF levels [ 75 ]. On the other hand, there are several reports showing an increase in serum BDNF levels and also improvement in cognitive performance in PD patients, who underwent cognitive rehabilitation, when compared to a placebo group.
These findings suggest that serum BDNF levels may represent a biomarker for the effects of cognitive rehabilitation in PD patients affected with mild cognitive impairment [ 76 ].
Aging is another important variable that not only leads to the slow progression of PD but also hampers the medical treatment response [ 77 ]. There is aging without PD, but there is no PD without aging [ 78 ], showing decreased dopamine levels, increased sensitivity to mitochondrial dysfunction, alterations in calcium channel activity, accumulation of iron and neuromelanin, changes in protein degradation pathways [ 79 ], striatal spine retraction [ 80 ] and loss of striatal spine density [ 81 ].
In PD patients, aging leads to severe gait disturbances including musculoskeletal rigidity, axial impairment and age-related dementia [ 85 ]. In the brain, next to nigrostriatal pathway, hippocampus is highly sensitive to aging and BDNF is critically involved in the regulation of age-related hippocampal decline [ 86 ].
Cacquevel, M. Ageing and amyloid-beta peptide deposition contribute to an impaired brain tissue plasminogen activator activity by different mechanisms. Calabrese, F. Reduced neuroplasticity in aged rats: a role for the neurotrophin brain-derived neurotrophic factor. Aging 34, — Neuronal plasticity: a link between stress and mood disorders.
Psychoneuroendocrinology 34 Suppl. Caldeira, M. Cell Neurosci. Cammisuli, D. Cao, B. Reduced hippocampus volume and memory performance in bipolar disorder patients carrying the BDNF val66met met allele.
Carlino, D. Low serum truncated-BDNF isoform correlates with higher cognitive impairment in schizophrenia. Cirulli, F. Intrahippocampal administration of BDNF in adult rats affects short-term behavioral plasticity in the Morris water maze and performance in the elevated plus-maze. Hippocampus 14, — Clark, P. Colcombe, S. Fitness effects on the cognitive function of older adults: a meta-analytic study.
Combarros, O. Cotman, C. Exercise: a behavioral intervention to enhance brain health and plasticity. Physical activity and the maintenance of cognition: learning from animal models.
Alzheimers Dement. Counts, S. Noradrenaline activation of neurotrophic pathways protects against neuronal amyloid toxicity. Cracchiolo, J. Chan, C. Sex differences in brain-derived neurotrophic factor signaling and functions. Chang, Y. Chapman, T. Aging and infection reduce expression of specific brain-derived neurotrophic factor mRNAs in hippocampus. Aging 33, Charlton, R. The relationship between episodic long-term memory and white matter integrity in normal aging.
Neuropsychologia 48, — Chen, W. Cheng, B. Churchill, J. Exercise, experience and the aging brain. Danckert, S. Does aging affect recall more than recognition memory? Aging 28, — Dempster, E. Association between BDNF val66 met genotype and episodic memory. B Neuropsychiatr. Deng, P. Engineered BDNF producing cells as a potential treatment for neurologic disease.
Expert Opin. Dennis, N. Brain-derived neurotrophic factor val66met polymorphism and hippocampal activation during episodic encoding and retrieval tasks. Hippocampus 21, — Devi, L.
Neuropsychopharmacology 37, — Dey, N. Di Lazzaro, V. BDNF plasma levels in acute stroke. Dias, V. Cognitive function and serum levels of brain-derived neurotrophic factor in patients with bipolar disorder. Bipolar Disord. Dietrich, M. Exercise-induced synaptogenesis in the hippocampus is dependent on UCP2-regulated mitochondrial adaptation.
Ding, Q. Insulin-like growth factor I interfaces with brain-derived neurotrophic factor-mediated synaptic plasticity to modulate aspects of exercise-induced cognitive function. Dodds, C. Overestimation of the effects of the BDNF val66met polymorphism on episodic memory-related hippocampal function: a critique of a recent meta-analysis. Drapeau, E. Spatial memory performances of aged rats in the water maze predict levels of hippocampal neurogenesis. Stem cell review series: role of neurogenesis in age-related memory disorders.
Aging Cell 7, — Driscoll, I. Longitudinal pattern of regional brain volume change differentiates normal aging from MCI. Neurology 72, — The aging hippocampus: cognitive, biochemical and structural findings.
Cortex 13, — Plasma BDNF is associated with age-related white matter atrophy but not with cognitive function in older, non-demented adults. PLoS One 7:e Duman, R. A neurotrophic model for stress-related mood disorders.
Psychiatry 59, — Durany, N. Duzel, E. Can physical exercise in old age improve memory and hippocampal function? Brain , — Dwivedi, Y. Altered gene expression of brain-derived neurotrophic factor and receptor tyrosine kinase B in postmortem brain of suicide subjects.
Psychiatry 60, — Eadie, B. Voluntary exercise alters the cytoarchitecture of the adult dentate gyrus by increasing cellular proliferation, dendritic complexity, and spine density. Egan, M. Cell , — Einoch, R. Elliott, E. Brain-derived neurotrophic factor induces a rapid dephosphorylation of tau protein through a PI-3 Kinase signalling mechanism. Erickson, C. The neurobiology of memory changes in normal aging.
Erickson, K. The aging hippocampus: interactions between exercise, depression, and BDNF. Neuroscientist 18, 82— Brain-derived neurotrophic factor is associated with age-related decline in hippocampal volume.
Exercise training increases size of hippocampus and improves memory. Ernfors, P. Molecular cloning and neurotrophic activities of a protein with structural similarities to nerve growth factor: developmental and topographical expression in the brain.
Fahnestock, M. Future Neurol. BDNF increases with behavioral enrichment and an antioxidant diet in the aged dog. Aging 33, — Fernandes, B. Peripheral brain-derived neurotrophic factor in schizophrenia and the role of antipsychotics: meta-analysis and implications.
Psychiatry 20, — Ferris, L. The effect of acute exercise on serum brain-derived neurotrophic factor levels and cognitive function. Sports Exerc. Fink, K. Finkel, D. The longitudinal relationship between processing speed and cognitive ability: genetic and environmental influences. Fischer, W. Fisher, M. Neuroscience-informed auditory training in schizophrenia: a final report of the effects on cognition and serum brain-derived neurotrophic factor.
Flicker, C. Mild cognitive impairment in the elderly: predictors of dementia. Neurology 41, — Google Scholar. Forlenza, O. Effect of brain-derived neurotrophic factor Val66Met polymorphism and serum levels on the progression of mild cognitive impairment. World J. Psychiatry 11, — Francis, B. Frick, K. Use it or lose it: environmental enrichment as a means to promote successful cognitive aging.
ScientificWorldJournal 10, — Friedland, R. Friedman, W. Proneurotrophins, seizures, and neuronal apoptosis. Neuroscientist 16, — Fukumoto, N. Fumagalli, F. Pharmacogenomics J. Gajewski, P. Neuropsychologia 50, — Gallo, F.
Immediate early genes, memory and psychiatric disorders: focus on c-Fos, egr1 and arc. Gamiz, F. Spontaneous object recognition memory in aged rats: complexity versus similarity. Garcia-Mesa, Y. Psychoneuroendocrinology 45, — Garcia, R. Stress, synaptic plasticity, and psychopathology. Garza, A. Gillen, J. Is high-intensity interval training a time-efficient exercise strategy to improve health and fitness?
Giuffrida, M. Beta-amyloid monomers are neuroprotective. Aging 10, — Glasky, A. Effect of AIT, a purine analog, on working memory in normal and aged mice. Goldberg, T. Gooney, M. Aging 25, — Granger, R. Facilitation of glutamate receptors reverses an age-associated memory impairment in rats.
Synapse 22, — Green, C. Exercising your brain: a review of human brain plasticity and training-induced learning.
Greene, E. Degeneration of hippocampal fibers and spatial memory deficit in the aged rat. Aging 8, 35— Greenough, W. Possible memory storage differences among mice reared in environments varying in complexity. Gregory, S. Physical activity, cognitive function, and brain health: what is the role of exercise training in the prevention of dementia? Brain Sci. Griesbach, G. Voluntary exercise following traumatic brain injury: brain-derived neurotrophic factor upregulation and recovery of function.
Guimond, S. Psychiatry Res. Neuroimaging , 50— Haapasalo, A. Hall, C. Cognitive activities delay onset of memory decline in persons who develop dementia. Neurology 73, — Hansell, N. Genes Brain Behav. Hariri, A. Brain-derived neurotrophic factor val66met polymorphism affects human memory-related hippocampal activity and predicts memory performance.
Harris, S. The genetics of cognitive ability and cognitive ageing in healthy older people. Trends Cogn. The brain-derived neurotrophic factor Val66Met polymorphism is associated with age-related change in reasoning skills. Harrisberger, F. The association of the BDNF Val66Met polymorphism and the hippocampal volumes in healthy humans: a joint meta-analysis of published and new data. Harrison, P. The emerging neurobiology of bipolar disorder. Haworth, C.
The heritability of general cognitive ability increases linearly from childhood to young adulthood. Psychiatry 15, — Hayashi, M. Changes in BDNF-immunoreactive structures in the hippocampal formation of the aged macaque monkey. Sequential mRNA expression for immediate early genes, cytokines, and neurotrophins in spinal cord injury. Neurotrauma 17, — Hayes, V. Organization, sequence and functional analysis of a mouse BDNF promoter. Heffernan, J. Heitz, U. Plasma and serum brain-derived neurotrophic factor BDNF levels and their association with neurocognition in at-risk mental state, first episode psychosis and chronic schizophrenia patients.
Psychiatry 25, 1— Heldt, S. Hippocampus-specific deletion of BDNF in adult mice impairs spatial memory and extinction of aversive memories. Psychiatry 12, — Hillman, C. Be smart, exercise your heart: exercise effects on brain and cognition. Hock, C. Region-specific neurotrophin imbalances in Alzheimer disease: decreased levels of brain-derived neurotrophic factor and increased levels of nerve growth factor in hippocampus and cortical areas.
Hofer, M. Regional distribution of brain-derived neurotrophic factor mRNA in the adult mouse brain. Hoffman, A. Recovery after chronic stress within spatial reference and working memory domains: correspondence with hippocampal morphology.
Hoffmann, K. Holden, H. Less efficient pattern separation may contribute to age-related spatial memory deficits. Hopkins, M. BDNF expression in perirhinal cortex is associated with exercise-induced improvement in object recognition memory. Physical exercise during adolescence versus adulthood: differential effects on object recognition memory and brain-derived neurotrophic factor levels. Neuroscience , 84— Horch, H.
BDNF release from single cells elicits local dendritic growth in nearby neurons. Hori, H. Relationships between serum brain-derived neurotrophic factor, plasma catecholamine metabolites, cytokines, cognitive function and clinical symptoms in Japanese patients with chronic schizophrenia treated with atypical antipsychotic monotherapy. Psychiatry 18, — Horn, J. Age differences in primary mental ability factors. Houlihan, L. Replication study of candidate genes for cognitive abilities: the Lothian Birth Cohort Hsiao, Y.
Hsu, C. Expression of immediate early gene and growth factor mRNAs in a focal cerebral ischemia model in the rat. Stroke 24, I78—I Huang, E. Neurotrophins: roles in neuronal development and function.
Hundley, W. Cardiac cycle-dependent changes in aortic area and distensibility are reduced in older patients with isolated diastolic heart failure and correlate with exercise intolerance. Intlekofer, K.
Iritani, S. Immunohistochemical study of brain-derived neurotrophic factor and its receptor, TrkB, in the hippocampal formation of schizophrenic brains. Psychiatry 27, — Issa, G. An inverse relationship between cortisol and BDNF levels in schizophrenia: data from human postmortem and animal studies.
Jack, CR. Neurology 51, — Jayaweera, H. Episodic memory in depression: the unique contribution of the anterior caudate and hippocampus. Jiang, X. The excitoprotective effect of N-methyl-D-aspartate receptors is mediated by a brain-derived neurotrophic factor autocrine loop in cultured hippocampal neurons.
Jobst, K. Lancet , — Jones, T. Conjunction errors in recognition memory: modality-free errors for older adults but not for young adults. Acta Psychol. Joyce, N. Mesenchymal stem cells for the treatment of neurodegenerative disease. Kailainathan, S. Kambeitz, J.
Effect of BDNF val 66 met polymorphism on declarative memory and its neural substrate: a meta-analysis. Karnik, M. BDNF polymorphism rs and hippocampal structure and memory performance in healthy control subjects. Katoh-Semba, R. Riluzole enhances expression of brain-derived neurotrophic factor with consequent proliferation of granule precursor cells in the rat hippocampus. Brain-derived neurotrophic factor and inflammatory markers in patients with early- vs.
Kennedy, K. BDNF val66met polymorphism affects aging of multiple types of memory. Kerschensteiner, M. Activated human T cells, B cells, and monocytes produce brain-derived neurotrophic factor in vitro and in inflammatory brain lesions: a neuroprotective role of inflammation?
Kesslak, J. Learning upregulates brain-derived neurotrophic factor messenger ribonucleic acid: a mechanism to facilitate encoding and circuit maintenance? Kidd, S. Direct evidence of mesenchymal stem cell tropism for tumor and wounding microenvironments using in vivo bioluminescent imaging. Stem Cells 27, — Kim, D. Kim, E.
Stress effects on the hippocampus: a critical review. Kim, H. Symptoms of depression and the discrepancy between implicit and explicit self-esteem. Psychiatry 63, 1—5. Kim, J. Stress: metaplastic effects in the hippocampus. Kim, S. Memory, visual discrimination performance, and the human hippocampus.
Kiprianova, I. Brain-derived neurotrophic factor prevents neuronal death and glial activation after global ischemia in the rat. Kleim, J. BDNF val66met polymorphism is associated with modified experience-dependent plasticity in human motor cortex. Klein, A. Kollen, M. Aging 31, — Kosse, N. Effectiveness and feasibility of early physical rehabilitation programs for geriatric hospitalized patients: a systematic review. BMC Geriatr. Kremen, W.
Genetics of verbal working memory processes: a twin study of middle-aged men. Neuropsychology 21, — Kronenberg, G. Physical exercise prevents age-related decline in precursor cell activity in the mouse dentate gyrus. Aging 27, — Kumar, A. Long-term potentiation at CA3-CA1 hippocampal synapses with special emphasis on aging, disease, and stress. Kunugi, H. Psychiatry 6, 83— Kwon, D. Exercise ameliorates cognition impairment due to restraint stress-induced oxidative insult and reduced BDNF level.
Laing, K. Age 34, — Lambert, J. Lapchak, P. Aging 14, — Larsen, M. Regulation of brain-derived neurotrophic factor BDNF in the chronic unpredictable stress rat model and the effects of chronic antidepressant treatment.
Larson, E. Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older. Laske, C. Lauterborn, J. Transcript-specific effects of adrenalectomy on seizure-induced BDNF expression in rat hippocampus.
Chronic elevation of brain-derived neurotrophic factor by ampakines. Lee, J. Spatial learning deficits in the aged rat: neuroanatomical and neurochemical correlates. Lee, R. Regulation of cell survival by secreted proneurotrophins. Science , — Lee, S. Ischemic preconditioning enhances neurogenesis in the subventricular zone.
Lessmann, V. Neurotrophin secretion: current facts and future prospects. Lessov-Schlaggar, C. Lancet , — Zuccato, C. Baquet, Z. Early striatal dendrite deficits followed by neuron loss with advanced age in the absence of anterograde cortical brain-derived neurotrophic factor. Gauthier, L. Huntingtin controls neurotrophic support and survival of neurons by enhancing BDNF vesicular transport along microtubules.
Strand, A. Expression profiling of Huntington's disease models suggests that brain-derived neurotrophic factor depletion plays a major role in striatal degeneration. Zala, D. Progressive and selective striatal degeneration in primary neuronal cultures using lentiviral vector coding for a mutant huntingtin fragment. Canals, J. Brain-derived neurotrophic factor regulates the onset and severity of motor dysfunction associated with enkephalinergic neuronal degeneration in Huntington's disease.
Simmons, D. Up-regulating BDNF with an ampakine rescues synaptic plasticity and memory in Huntington's disease knockin mice. This article reported that ampakines increase BDNF expression in the brain and reduce deficits in a transgenic mouse model of Huntington's disease.
Article PubMed Google Scholar. Kells, A. Gene Ther. Kaplan, D. Neurotrophin signal transduction in the nervous system. Wijesekera, L. Amyotrophic lateral sclerosis. Orphanet J. Rare Dis. Neuroscience 71 , — Giehl, K. Mitsumoto, H. Neurology 52 , — Beck, M.
Lateral Scler. Other Motor Neuron Disord. Ochs, G. Ankeny, D. Pegylated brain-derived neurotrophic factor shows improved distribution into the spinal cord and stimulates locomotor activity and morphological changes after injury.
Pardridge, W. Combined use of carboxyl-directed protein pegylation and vector-mediated blood—brain barrier drug delivery system optimizes brain uptake of brain-derived neurotrophic factor following intravenous administration. Doyle, K. Mechanisms of ischemic brain damage. Neuropharmacology 55 , — Ferrer, I. Brain-derived neurotrophic factor reduces cortical cell death by ischemia after middle cerebral artery occlusion in the rat.
Muller, H. Brain-derived neurotrophic factor but not forced arm use improves long-term outcome after photothrombotic stroke and transiently upregulates binding densities of excitatory glutamate receptors in the rat brain. Stroke 39 , — Larsson, E. Evidence for neuroprotective effects of endogenous brain-derived neurotrophic factor after global forebrain ischemia in rats. Blood Flow Metab. Huang, E. Neurotrophins: roles in neuronal development and function.
Gordon, T. Experimental strategies to promote functional recovery after peripheral nerve injuries. Tobias, C. Delayed grafting of BDNF and NT-3 producing fibroblasts into the injured spinal cord stimulates sprouting, partially rescues axotomized red nucleus neurons from loss and atrophy, and provides limited regeneration. Blesch, A. Transient growth factor delivery sustains regenerated axons after spinal cord injury. Lu, P. Neurotrophism without neurotropism: BDNF promotes survival but not growth of lesioned corticospinal neurons.
Stokols, S. Freeze-dried agarose scaffolds with uniaxial channels stimulate and guide linear axonal growth following spinal cord injury. Biomaterials 27 , — Spinal cord injury: plasticity, regeneration and the challenge of translational drug development. Trends Neurosci. Alto, L. Chemotropic guidance facilitates axonal regeneration and synapse formation after spinal cord injury. Hollis, E. Induction of corticospinal regeneration by lentiviral trkB-induced Erk activation.
Plunet, W. Dietary restriction started after spinal cord injury improves functional recovery. Ying, Z. BDNF-exercise interactions in the recovery of symmetrical stepping after a cervical hemisection in rats.
Neuroscience , — Schumacher, J. Evidence for a relationship between genetic variants at the brain-derived neurotrophic factor BDNF locus and major depression. Psychiatry 58 , — Post, R. Role of BDNF in bipolar and unipolar disorder: clinical and theoretical implications. Kato, M. Review and meta-analysis of antidepressant pharmacogenetic findings in major depressive disorder. Psychiatry 15 , — Campbell, S. Lower hippocampal volume in patients suffering from depression: a meta-analysis.
Psychiatry , — Dwivedi, Y. Altered gene expression of brain-derived neurotrophic factor and receptor tyrosine kinase B in postmortem brain of suicide subjects. Psychiatry 60 , — Brunoni, A. A systematic review and meta-analysis of clinical studies on major depression and BDNF levels: implications for the role of neuroplasticity in depression.
Vermetten, E. Long-term treatment with paroxetine increases verbal declarative memory and hippocampal volume in posttraumatic stress disorder. Psychiatry 54 , — Sen, S. Serum brain-derived neurotrophic factor, depression, and antidepressant medications: meta-analyses and implications.
Psychiatry 64 , — Shimizu, E. Alterations of serum levels of brain-derived neurotrophic factor BDNF in depressed patients with or without antidepressants. Psychiatry 54 , 70—75 Chen, B.
Increased hippocampal BDNF immunoreactivity in subjects treated with antidepressant medication. Psychiatry 50 , — Cotman, C. Exercise: a behavioral intervention to enhance brain health and plasticity.
Neeper, S. Physical activity increases mRNA for brain-derived neurotrophic factor and nerve growth factor in rat brain. Fuss, J. Hippocampus 20 , — PubMed Google Scholar. B Neuropsychiatr. Dempster, E. Association between BDNF val66 met genotype and episodic memory. Hariri, A. Brain-derived neurotrophic factor val66met polymorphism affects human memory-related hippocampal activity and predicts memory performance. Pezawas, L. The brain-derived neurotrophic factor val66met polymorphism and variation in human cortical morphology.
Erickson, K. Brain-derived neurotrophic factor is associated with age-related decline in hippocampal volume. Rybakowski, J. Pharmacogenomics 9 , — Sugiyama, N. Temporal changes in the expression of brain-derived neurotrophic factor mRNA in the ventromedial nucleus of the hypothalamus of the developing rat brain. Pelleymounter, M. Characteristics of BDNF-induced weight loss. Fox, E. A mechanism underlying mature-onset obesity: evidence from the hyperphagic phenotype of brain-derived neurotrophic factor mutants.
Rios, M. Conditional deletion of brain-derived neurotrophic factor in the postnatal brain leads to obesity and hyperactivity. Gray, J. Hyperphagia, severe obesity, impaired cognitive function, and hyperactivity associated with functional loss of one copy of the brain-derived neurotrophic factor BDNF gene.
Diabetes 55 , — Yeo, G. A de novo mutation affecting human TrkB associated with severe obesity and developmental delay. Tonra, J. Diabetes 48 , — Ono, M. Intermittent administration of brain-derived neurotrophic factor ameliorates glucose metabolism in obese diabetic mice. Metabolism 49 , — Fujinami, A. Serum brain-derived neurotrophic factor in patients with type 2 diabetes mellitus: relationship to glucose metabolism and biomarkers of insulin resistance.
Winkler, J. Reversible Schwann cell hyperplasia and sprouting of sensory and sympathetic neurites after intraventricular administration of nerve growth factor. Williams, L. Hypophagia is induced by intracerebroventricular administration of nerve growth factor. Eriksdotter Jonhagen, M.
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