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BDNF

BDNF

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BDNF (Brain-Derived Neurotrophic Factor) is not a hormone, but a protein and neurotrophin. It acts as a growth factor (neurotrophic factor) in the brain. Learning requires neurotrophic factors.

BDNF influences brain development, synaptic plasticity, learning, memory, neuronal survival and other neuronal processes. BDNF is elevated during early development and promotes the maturation and function of the hippocampus and cortex.
BDNF is involved in various disorders such as depression, schizophrenia, Alzheimer’s disease, dementia, Huntington’s disease, eating disorders, Rett syndrome and epilepsy.

Whether BDNF is altered in ADHD is unclear.
Stimulant treatment increases levels of BDNF and other neurotrophic factors, which improves the ability to learn (not only school or lecture material, but also meaningful changes in one’s behavior as a result of an experience). Endurance exercise also increases BDNF. Taurine increases BDNF in the striatum.
BDNF can be influenced by factors such as learning processes, antidepressants, physical activity, dietary restriction, light and sensory stimulation.
The effect of BDNF can be altered by stress, with chronic stress reducing BDNF levels in the hippocampus and increasing them in the nucleus accumbens.

There are different receptors for BDNF, including the TrkB receptor, which has a high affinity for BDNF, and the p75 receptor, which has a low affinity for BDNF.
BDNF can freely cross the blood-brain barrier.123 The BDNF blood serum level is said to correlate with the size of the hippocampus.4

BDNF is the most common and most widespread growth factor in the brain.5 The highest BDNF levels are found in the brain regions involved in attention and cognition:6

  • Hippocampus
  • frontal cortex
  • Amygdala

Other neurotrophins:7

  • NGF, nerve growth factor
    • Main receptor: TrkA
    • Neuronal differentiation, survival of cholinergic neurons, nociception
    • Development of the peripheral and central nervous system
  • Neurotrophin 3
    • Main receptor: rkC (TrkB)
    • Development of proprioceptive neurons, maturation of oligodendrocytes
    • Development of the spinal cord and sensory neurons
    • possibly increased with ADHD8
  • Neurotrophin 4/5
    • Main receptor: TrkB
    • Overlapping functions with BDNF, neuromuscular development
    • Supports the maintenance of synapses during development
  • Neurotrophin 6
  • CNTF, Ciliary Neurotrophic Factor
  • GDNF, Glial Cell Line-derived Neurotrophic Factor
    • Main receptor: RET (via GFRα1 co-receptor)
    • Promotes the survival of dopaminergic and motor neurons, kidney development
    • Crucial for the maturation of the enteric nervous system and motor neurons
    • possibly increased with ADHD8
  • IGF-1, insulin-like growth factor
  • FGF, fibroblast growth factor
  • TGF-beta Transforming Growth Factor
  • Sonic Hedgehog
  • proNGF
    • Precursor protein of NGF
    • eliminates damaged neurons
  • VEGF, Vascular Endothelial Growth Factor
    • stimulates angiogenesis, among other things

1. Control areas of BDNF

BDNF exists in two forms: proBDNF, from which mBDNF (mature BDNF) is produced by proteolytic cleavage5
While mBDNF as a growth factor promotes the survival, growth and plasticity of neurons, proBDNF supports apoptosis (cell death) and synaptic pruning (breakdown of synapses)
A healthy brain depends on an appropriate balance between proBDNF and BDNF.
If studies do not differentiate this, BDNF usually refers to mBDNF,

1.1. Behavioral functions

BDNF controls many behavioral functions in cooperation with serotonin.

BDNF influenced:9

  • Brain development
  • neurogenesis
    • Differentiation of hippocampal neuron precursors10
  • Processes of neuronal plasticity
    • Direct
      • Cellular processes of neuronal plasticity
    • Indirect
      • Effect on other plasticity-modifying processes
    • Short term
      • Potentiation of synaptic excitation transmission through the depolarization of postsynaptic nerve cells
      • Facilitates the release of presynaptic neurotransmitters
    • Long-term
      • Persistent change in cell excitability and synaptic plasticity11
  • Activity-dependent synaptic plasticity1210
    • synaptogenesis between Ia afferents and motor neurons10
  • memory consolidation13
    • The long-term potentiation (LTP) underlying learning and memory14
    • Deactivation of the BDNF gene or the BDNF receptor in mice
      • Restricts their learning behavior15 whereby the learning time required for spatial learning was doubled16
      • Impairs long-term potentiation, which is essential for long-term memory15
      • Prevents the improvement of learning through endurance training17
      • These effects can be remedied by an external supply of BDNF11
    • GABA inhibits long-term potentiation18
  • the sensitization of nociceptive fibres10
  • visceral sensory innervation, respiratory control10

BDNF promotes hippocampal function, in particular the survival of newly formed granule cells throughout adult life.19 BDNF modulates hippocampal plasticity and hippocampus-dependent memory.20

The transcription factor Cyclic AMP response element-binding protein (CREB1) is an important regulator of BDNF-induced gene expression. BDNF stimulates the phosphorylation and activation of CREB in nerve cells.21

BDNF influences the glutamate metabolism in the brain. In around 30 % of nerve cells, glutamatergic synaptic transmission is increased by 100 ng / ml each22

  • BDNF by 143 %
  • Neurotrophin-4/5 by 170 %

cAMP rapidly increases neurotrophin-3 (= BNDF-/NT-3 = tropomyosin receptor kinase B (TrkB) = tyrosine receptor kinase B) and causes BDNF-dependent long-term potentiation in the hippocampus.23

1.2. Disorders

BDNF is involved in various disorders, e.g.

  • Depression24
    • BDNF decreases in the hippocampus
    • BDNF increased in the nucleus accumbens25
    • BDNF decreases in blood plasma26
  • ADHD
    • Contradictory results, these below
  • Schizophrenia
  • Obsessive-compulsive disorder
  • Alzheimer’s24
    • BDNF reduces27
      • In the parietal cortex,28
      • In the hippocampus and temporal cortex29
      • In the entorhinal cortex30
    • NGF (Nerve Growth Factor) was higher in the dentate gyrus30
    • NT-3 was reduced in the motor cortex30
  • Dementia
  • Huntington’s disease
  • Eating disorders
    • Anorexia nervosa
    • Bulimia nervosa
  • Rett syndrome
  • Epilepsy

2. BDNF receptors

BDNF receptors are predominantly located in memory-relevant brain regions such as the PFC and hippocampus.12

2.1. TrkB receptor (TrkB)

The TrkB receptor has a high affinity for BDNF.12
It acts quickly (direct modulation of ion channels and synapses) and slowly (genetically).

2.2. Truncated TrkB receptor (TrkB-T)

2.3. P75 receptor

The p75 receptor has a low affinity for BDNF.12
It acts almost exclusively via slow, complex signaling cascades (genetic) and mediates apoptosis.

3. Change in BDNF

3.1. Stress and BDNF

3.1.1. Stress reduces BDNF in the hippocampus

Stress reduces BDNF31 and BDNF expression in the hippocampus of humans and rats. Chronic administration of antidepressants prevents this.32

BDNF was significantly reduced by singular33 such as repeated immobilization in the hippocampus and dentate gyrus, but not neurotrophin-4 or tyrosine receptor kinases (trkB or C).
In contrast, NT-3 was increased in the hippocampus and dentate gyrus, but only during repeated immobilization (chronic stress), which was probably primarily mediated by corticosterone.
The reduction in BDNF occurred (only in the dentate gyrus) even without a corticosterone response (in rats that had had their adrenal cortex removed and were therefore unable to secrete corticosterone).34

The reduction of BDNF due to stress in the hippocampus and the increase of BDNF due to stress in the paraventricular hypothalamus may decrease with age, while the changes in NGF (Nerve Growth Factor) and neurotrophin-3 (NT-3) do not appear to change with age.35

One study found that BDNF was reduced by chronic glucocorticoid administration in the PFC, but not in the dorsal hippocampus.36

3.1.2. Chronic stress increases BDNF in the nucleus accumbens

Chronic stress increases BDNF expression in the nucleus accumbens, which in turn correlates with depression-like behaviors, such as early passivity37 or social phobia38, but only in stress-prone rats, not in stress-resistant rats.39

BDNF is also elevated in the nucleus accumbens in people with depression.25

Stress also has significant effects on BDNF in the amygdala and PFC.19

Blocking eye activity drastically reduces BDNF in the visual cortex of the affected eye.24

3.1.3. Chronic / acute stress and gender

In female rats, chronic stress decreased BDNF in prelimbic areas of the PFC, while acute stress increased BDNF in the dentate gyrus. In males, the values remained unchanged in both cases40
BDNF is also involved in the impairment of dopamine signaling during early infant stress caused by maternal deprivation in rats.41

3.1.4. BDNF for DAT deficiency

DAT-KO mice that do not produce dopamine transporters show massive changes in BDNF in PFC and striatum:

  • In the PFC
    • Reduced BDNF gene expression42
    • Total BDNF and BDNF exon IV mRNA levels reduced43
    • MRNA levels of BDNF exon VI unchanged43
    • Reduced mBDNF levels and reduced trkB activation43
    • Reduced activation of αCaMKII in the PFC43
  • In the dorsolateral striatum
    • MBDNF level increased in the homogenate43
    • MBDNF levels in the cytosol increased43
    • MBDNF levels in the postsynaptic density are reduced.43
    • TrkB expression in the dorsolateral striatum postsynaptically reduced43
      • TrkB is a high-affinity BNDF receptor

3.2. What else influences BDNF

BDNF is increased by31

  • Learning processes
  • Enriched environment / complex environments44
    • Varied, stimulating environments increase BDNF in rats
  • Antidepressants
  • Physical activity
    • Endurance sports significantly increase BDNF levels in the hippocampus and cerebral cortex.454647
    • Chronic estrogen deficiency of 7 weeks (but not acute estrogen deficiency of 3 weeks) reduces the increase of BDNF by endurance exercise in mice.48
  • Dietary restriction increases BDNF in the dentate gyrus49
  • Light and the circadian rhythm of daylight alter BDNF and neurotrophin-3.
    • In darkness, BDNF is high in the hippocampus (minimum 3.5 in light, maximum 17 in darkness)5051 in the cerebellum 52 and in the suprachiasmatic nucleus (SCN). In the SCN, BDNF levels were highest at dusk and dawn. In constant darkness, a BDNF rhythm was observed in the SCN, but not in the hippocampus.53
    • Light increases, darkness decreases BDNF in the visual cortex,54 the retina and superior colliculi52 as well as in the cerebral cortex. At least in the cerebral cortex, this rhythm is modulated by noradrenaline.55
  • Sensory stimulation of tactile hairs increases BDNF in the primary sensory cortex (barrel cortex).5657
  • Taurine significantly increased BDNF levels in the striatum in both SHR and WKY rats (whether low or high dose).58

4. Gene variants of BDNF

BDNF Val/Met correlated in humans, compared to BDNF Val/Val, with

  • A poorer episodic memory
  • Abnormal hippocampal activation on fMRI
  • Less N-acetyl-aspartate (NAA) in the hippocampus.20

5. BDNF and other growth factors and dopamine

BDNF improves the survival and growth of7

  • serotonergic neurons
  • dopaminergic neurons
  • cholinergic neurons.

BDNF promotes the formation of dendritic spines, which are important for memory and cognitive flexibility. Disorders of BDNF signaling are associated with impaired synaptic structure, memory deficits and an increased risk of neurodevelopmental disorders.7

5.1. BDNF regulates dopamine in the striatum

This presentation is based on Sulzer et al 59

The neurotrophic factor BDNF acts on TrkB (and P75) receptors.
Genetic elimination (BDNF-/- mice) or strong reduction of BDNF (BDNF-/+ mice) in the brain causes6061

  • evoked dopamine release
    • significantly reduced in the NAc shell
    • significantly reduced in the dorsal striatum
    • unchanged in the NAc core
  • dramatically increased consumption of high-fat food (intake of normal food unchanged)
  • normalized consumption of high-fat food due to D1 receptor agonists
  • extracellular dopamine levels in the caudate nucleus / putamen more than doubled
  • increased increase in dopamine levels after potassium stimulation (120 mM) (10-fold) compared to wild-type controls (6-fold)
  • electrically evoked dopamine release as well as the dopamine uptake rate in the caudate nucleus / putamen reduced

BDNF administration

  • increases the DA overflow in the striatum evoked by depolarization
  • can partially restore electrically evoked dopamine in BDNF-/+ mice
  • leaves extracellular dopamine levels unchanged

5.2. GDNF regulates dopamine release and dopamine uptake in the striatum

This presentation is based on Sulzer et al 59

The neurotrophic factor GDNF can regulate striatal DA release and uptake. GDNF plays a key role in the development, maintenance and regeneration of the mesostriatal DA system.62
In vivo, GDNF injection into the NAc caused an increase in K+-triggered DA release in the caudate nucleus/putamen63 via a long-lasting increase in TH phosphorylation and presumably DA synthesis in the striatum and SNc64
GDNF increases the amount of DA released from vesicles in axonal varicosities of midbrain DA neurons.65
GDNF increases the number of DA neurons in the midbrain and terminals in the striatum, thereby increasing dopamine in the striatum.66
GDNF regulates DAT surface expression via its receptor (Ret) by means of the guanine nucleotide exchange factor protein VAV2 (from the Rho family). Mice lacking Vav2 or Ret show increased DAT activity in the NAc.66

6. BDNF altered in ADHD?

6.1. BDNF for ADHD

The study situation on BDNF in ADHD is contradictory. There appears to be no systematic change in BDNF in ADHD. There may be a gender-specific increase only in boys.
This could also be due to the measurement methods used. Serum measurements of BDNF show less variability than plasma measurements.7
BDNF is subject to a diurnal cycle. The values are at their highest early in the morning and fall until the evening.

BDNF reduced (7 studies, 2 reviews)

  • Blood serum
    • Decreased in children with ADHD-HI and ADHD-C in the morning and evening, in children with ADHD-I only decreased in the evening; blood serum67
    • in adults with ADHD-I and ADHD-C; lower in ADHD-C than in ADHD-I; blood serum68
    • reduced in drug-naïve children with ADHD; lower in ADHD-I than in ADHD-C; blood serum69
    • reduced in children with ADHD, blood serum70
  • Blood plasma
    • significantly decreased in children with ADHD-H compared to controls (unchanged in ADHD-C and tendentially increased in ADHD-HI); no gender differences; blood plasma71
    • significantly reduced in untreated children of all ADHD presentations; blood plasma72
    • significantly decreased in children of all ADHD presentation forms, regardless of ODD comorbidity, blood plasma morning73
  • reduced (Review74’
  • reduced (Review)75

BDNF increased (7 studies, 1 meta-analysis)

  • Blood serum
    • in children with ADHD, as well as NGF, GDNF, galanin; blood serum76
    • increased in children, especially in older age, lower IQ and inattention; blood serum77
  • Blood plasma
    • gender-dependent increase in Chinese children with ADHD; blood plasma78
    • BDNF increased in children with ADHD, blood plasma79
    • tends to be increased in children with ADHD-HI compared to controls (unchanged in ADHD-C and decreased in ADHD-I); no gender differences; blood plasma71
    • Elevated BDNF and elevated sialic acid levels correlated with ADHD and eveningness in drug-free children; blood plasma80
    • increased, without significant differences between the subtypes; blood plasma81
  • increased in the blood of male persons with ADHD, unchanged in women (meta-analysis, k = 10, n = 1,183)82

BDNF unchanged (5 studies, 1 meta-analysis)

  • Blood serum
    • no correlation between blood levels of the growth factor BDNF and ADHD (n = 2,307); blood serum83
    • BDNF, NT-3, NGF and FGF-2 (fibroblast growth factor-2) unchanged in ADHD; blood serum84
    • BDNF and NGF in blood serum unchanged, GDNF and NTF3 increased. No correlations between serum neurotrophin levels and ADHD severity8
    • unchanged85
  • Blood plasma
    • unchanged in children with ADHD-C compared to controls (decreased in ADHD-I and tendentially increased in ADHD-HI); no gender differences; blood plasma71
  • no change (meta-analysis, k = 19)86

The BDNF polymorphism Val66Met correlated with:87

  • reduced volume of gray matter in PFC and limbic structures88
  • altered connectivity of the default mode network in people with ADHD89

BDNF-KO mice show strong hyperactivity9091 92 and obesity91. Heterozygous BDNF-KO mice (= reduced BDNF) also show hyperactivity and obesity.93

6.2. Alteration of BDNF by ADHD medication

Here, too, the study situation is inconsistent.

MPH increased BDNF (5 studies, 1 animal study)

  • MPH increased BDNF94 in the dorsal striatum only in male rats and in the nucleus accumbens regardless of sex.9596
  • MPH significantly increased BDNF in children with ADHD-C, above that of controls; in ADHD-I baseline lower than ADHD-C, but no increase due to MPH; blood serum69
  • Chronic MPH administration (1 to 3 mg/kg) increased BDNF mRNA expression in muscleblind-like 2 (Mbnl2) knockout mice97
  • Combined MPH/fluoxetine administration during adolescence increased BDNF expression in the ventral tegmentum of adult rats98
  • Rats that received MPH as young animals had higher levels of BDNF in the PFC as they aged.99

reduced (3 studies)

  • MPH did not alter BDNF in ADHD-HI and ADHD-C, while MPH decreased BDNF in ADHD-I100
  • MPH reduced the previously elevated blood serum levels of BDNF, NGF, GDNF and galanin.76
  • MPH significantly reduced BDNF in the striatum of female rats by 42 % and significantly increased it in the striatum of male rats by 50.4 %. BDNF in the nucleus accumbens was unchanged.101

unchanged (1 meta-analysis, 1 animal study)

  • no change (meta-analysis)86
  • One study found no relevant influence of MPH on BDNF receptor expression in rats102
    differentiating (3 studies)
  • An increase or decrease in BDNF due to MPH could be age-dependent.103104
  • One study compared the effect of atomoxetine and methylphenidate on BDNF:105
    • Atomoxetine
      • increased BDNF mRNA levels
        • in the hippocampus
        • in the PFC
          • Total and exon IV BDNF mRNA levels increased
          • via increased AKT and GSK3β phosphorylation
    • Methylphenidate
      • increased BDNF gene expression
        • in the nucleus accumbens
        • in the Caudat putamen
      • reduced BDNF gene expression
        • in the PFC
        • via reduced synaptic levels of trkB, the high-affinity BDNF receptor, and reduced ERK1/2 activation
  • Atomoxetine reduced BDNF levels in adults with ADHD only in the ADHD-I group.106
  • In the dentate gyrus, only MPH, but not atomoxetine, appears to increase synaptic plasticity in rats, whereby a very high dose of 10 mg/kg body weight was used here. This is 5 to 15 times the usual dose of medication.107

As a result, the effect of MPH on BDNF seems to depend on the genetic circumstances, the time of MPH administration, age, gender and brain region.

6.3. Other growth factors in ADHD

The blood serum levels of VEGF (vascular endothelial growth factor) were significantly reduced in a study on ADHD, while those of GDNF (glial-derived neurotrophic factor) were significantly increased. However, their blood values did not correlate with the symptom severity of ADHD.84 Two studies found no altered blood serum levels of VEGF,108109 or IGF-1 or HIF-1α in children with ADHD.

In rats, MPH was associated with a significant increase in GDNF in the striatum and nucleus accumbens, irrespective of gender.95

7. Epigenetic influence of HDAC on BDNF

HDACs (histone deacetylases) cause a more compact DNA structure (chromatin), which reduces the expression of BDNF. HDAC inhibitors thus increase the expression of BDNF.

The universal HDAC inhibitor sulforaphane increased in vitro the levels of BDNF and components of the TrkB signaling cascade in mouse primary cortical neurons and in 3xTg-AD mice. The subsequent increase in acetylation of H3 and H4 near the P1 promoter of the BDNF gene led to increased levels of MAP2 and the synaptic proteins synaptophysin and PSD-95. Sulforaphane thus appears to have an epigenetic effect on BDNF.110

BDNF is also involved in the impairment of dopamine signaling during early childhood stress induced by maternal deprivation in rats. Early infant maternal deprivation increased HDAC2 and decreased H3K9ac. Subsequent elevation of the dendritic spine modulator AKAP150 decreased synaptic levels of protein kinase A and increased mBDNF. These effects were reversed in vivo by a single administration of the HDAC inhibitor CI-994.41

8. MBDNF/perBDNF ratio

One study found an increased proBDNF/mBDNF ratio in children with ADHD.70 Only in children with a history of febrile convulsions was proBDNF altered.
Since the ratio was only changed due to reduced BDNF levels and unchanged proBDNF levels compared to controls, this result should be viewed with caution in light of the very different study results on BDNF levels in ADHD (see above).

Reduced mBDNF levels due to inhibition of intracellular conversion from proBDNF correlated with:7

  • Disorders of episodic memory in animals111
  • Impairment of working memory and cognitive functions in epilepsy112

9. BDNF for ASS

In ASD, BDNF appears to correlate with abnormal brain growth, changes in connectivity and neuroinflammation in children. Reduced proBDNF has been reported in some drug-treated cases.7

  1. Sartorius, Hellweg, Litzke, Vogt, Dormann, Vollmay, Danker-Hopfe, Gass (2009): Correlations and discrepancies between serum and brain tissue levels of neurotrophins after electroconvulsive treatment in rats. Pharmacopsychiatry. 2009 Nov;42(6):270-6. doi: 10.1055/s-0029-1224162. PMID: 19924587. ↥

  2. Pan, Banks, Fasold, Bluth, Kastin (1998): Transport of brain-derived neurotrophic factor across the blood-brain barrier. Neuropharmacology. 1998;37(12):1553-1561. doi:10.1016/s0028-3908(98)00141-5 ↥

  3. Poduslo, Curran (1996): Permeability at the blood-brain and blood-nerve barriers of the neurotrophic factors: NGF, CNTF, NT-3, BDNF. Brain Res Mol Brain Res. 1996;36(2):280-286. doi:10.1016/0169-328x(95)00250-v ↥

  4. IMD-Labor: BDNF – ein Serum-Marker bei Depression und Burnout ↥

  5. Liu DY, Shen XM, Yuan FF, Guo OY, Zhong Y, Chen JG, Zhu LQ, Wu J (2015): The Physiology of BDNF and Its Relationship with ADHD. Mol Neurobiol. 2015 Dec;52(3):1467-1476. doi: 10.1007/s12035-014-8956-6. PMID: 25354496. REVIEW ↥ ↥

  6. Yeom CW, Park YJ, Choi SW, Bhang SY (2016): Association of peripheral BDNF level with cognition, attention and behavior in preschool children. Child Adolesc Psychiatry Ment Health. 2016 May 19;10:10. doi: 10.1186/s13034-016-0097-4. PMID: 27200107; PMCID: PMC4872344. ↥

  7. Panvino F, Paparella R, Tarani F, Lombardi C, Ferraguti G, Pisani F, Fiore M, Pancheva R, Ardizzone I, Tarani L (2025): Neurotrophins in Neurodevelopmental Disorders: A Narrative Review of the Literature. Int J Mol Sci. 2025 Aug 28;26(17):8335. doi: 10.3390/ijms26178335. PMID: 40943255; PMCID: PMC12428612. REVIEW ↥ ↥ ↥ ↥ ↥ ↥

  8. Bilgiç A, Toker A, Işık Ü, Kılınç İ (2017): Serum brain-derived neurotrophic factor, glial-derived neurotrophic factor, nerve growth factor, and neurotrophin-3 levels in children with attention-deficit/hyperactivity disorder. Eur Child Adolesc Psychiatry. 2017 Mar;26(3):355-363. doi: 10.1007/s00787-016-0898-2. PMID: 27561780. n = 154 ↥ ↥ ↥

  9. Zarrouki (2012): Die Wirkung des BDNF-Polymorphismus auf transkraniell induzierte Neuroplastizität, Dissertation ↥

  10. Huang EJ, Reichardt LF (2001): Neurotrophins: roles in neuronal development and function. Annu Rev Neurosci. 2001;24:677-736. doi: 10.1146/annurev.neuro.24.1.677. PMID: 11520916; PMCID: PMC2758233. REVIEW ↥ ↥ ↥ ↥ ↥

  11. Pearson-Fuhrhop, Kleim, Cramer (2009): Brain Plasticity and Genetic Factors, Topics in Stroke Rehabilitation, 16:4, 282-299, DOI: 10.1310/tsr1604-282 ↥ ↥

  12. Cunha, Brambilla, Thomas (2010): A simple role for BDNF in learning and memory? Front. Mol. Neurosci., 09 February 2010 | https://doi.org/10.3389/neuro.02.001.2010 ↥ ↥ ↥ ↥

  13. Figurov A, Pozzo-Miller LD, Olafsson P, Wang T, Lu B (1996): Regulation of synaptic responses to high-frequency stimulation and LTP by neurotrophins in the hippocampus. Nature. 1996 Jun 20;381(6584):706-9. doi: 10.1038/381706a0. PMID: 8649517. ↥

  14. Laske, Eschweiler (2006) Brain-derived neurotrophic factor: Vom Nervenwachstumsfaktor zum Plastizitätsmodulator bei kognitiven Prozessen und psychischen Erkrankungen. Der Nervenarzt, May 2006, Volume 77, Issue 5, pp 523–537 ↥

  15. Korte (2001): Lernen und Gedächtnis: Zelluläre und molekulare Grundlagen, Biologie in unserer Zeit, 31: 296-304. https://doi.org/10.1002/1521-415X(200109)31:5<296::AID-BIUZ296>3.0.CO;2-C ↥ ↥

  16. Linnarsson, Björklund, Ernfors (1997), Learning Deficit in BDNF Mutant Mice. European Journal of Neuroscience, 9: 2581-2587. doi:10.1111/j.1460-9568.1997.tb01687.x ↥

  17. Vaynman, Gomez‐Pinilla (2006): Revenge of the “Sit”: How lifestyle impacts neuronal and cognitive health through molecular systems that interface energy metabolism with neuronal plasticity. Neurosci. Res., 84: 699-715. https://doi.org/10.1002/jnr.20979 ↥

  18. Dubrovsky: Reconsidering Classifi cations of Depression Syndromes: Lessons from Neuroactive Steroids and Evolutionary Sciences; in: Weizman (Herausgeber) (2008): Neuroactive Steroids in Brain Function, Behavior and Neuropsychiatric Disorders: Novel Strategies for Research and Treatment; Chapter 19, S 385 ff ↥

  19. Feder, Nestler, Charney (2009): Psychobiology and molecular genetics of resilience. Nat Rev Neurosci. 2009 Jun; 10(6): 446–457. doi: 10.1038/nrn2649 PMC2833107. NIHMS174778 PMID: 19455174 ↥ ↥

  20. Egan, Kojima, Callicott, Goldberg, Kolachana, Bertolino, Zaitsev, Gold, Goldman, Dean, Lu, Weinberger (2003): The BDNF val66met polymorphism affects activity-dependent secretion of BDNF and human memory and hippocampal function. Cell. 2003 Jan 24;112(2):257-69. doi: 10.1016/s0092-8674(03)00035-7. PMID: 12553913. ↥ ↥

  21. Finkbeiner, Tavazoie, Maloratsky, Jacobs, Harris, Greenberg (1997): CREB: A Major Mediator of Neuronal Neurotrophin Responses, Neuron, Volume 19, Issue 5, 1997, Pages 1031-1047, ISSN 0896-6273, https://doi.org/10.1016/S0896-6273(00)80395-5. ↥

  22. Leßmann, Heumann (1998): Modulation of unitary glutamatergic synapses by neurotrophin-4/5 or brain-derived neurotrophic factor in hippocampal microcultures: presynaptic enhancement depends on pre-established paired-pulse facilitation, Neuroscience, Volume 86, Issue 2, 1998, Pages 399-413, ISSN 0306-4522, https://doi.org/10.1016/S0306-4522(98)00035-9. http://www.sciencedirect.com/science/article/pii/S0306452298000359 ↥

  23. Patterson, Pittenger, Morozov, Martin, Scanlin, Drake, Kandel (2001): Some Forms of cAMP-Mediated Long-Lasting Potentiation Are Associated with Release of BDNF and Nuclear Translocation of Phospho-MAP Kinase, Neuron, Volume 32, Issue 1, 2001, Pages 123-140, ISSN 0896-6273, https://doi.org/10.1016/S0896-6273(01)00443-3. http://www.sciencedirect.com/science/article/pii/S0896627301004433 ↥

  24. Lu (2003): BDNF and activity-dependent synaptic modulation. Learn Mem. 2003 Mar-Apr;10(2):86-98. ↥ ↥ ↥

  25. Krishnan, Han, Graham, Berton, Renthal, Russo, Laplant, Graham, Lutter, Lagace, Ghose, Reister, Tannous, Green, Neve, Chakravarty, Kumar, Eisch, Self, Lee, Tamminga, Cooper, Gershenfeld, Nestler (2007): Molecular adaptations underlying susceptibility and resistance to social defeat in brain reward regions. Cell. 2007 Oct 19;131(2):391-404. ↥ ↥

  26. Lee BH, Kim H, Park SH, Kim YK (2007): Decreased plasma BDNF level in depressive patients. J Affect Disord. 2007 Aug;101(1-3):239-44. doi: 10.1016/j.jad.2006.11.005. Epub 2006 Dec 13. PMID: 17173978. n = 172 ↥

  27. Hock C, Heese K, Hulette C, Rosenberg C, Otten U. 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. Arch Neurol. 2000 Jun;57(6):846-51. doi: 10.1001/archneur.57.6.846. PMID: 10867782. ↥

  28. Holsinger, Schnarr, Henry, Castelo, Fahnestock (2000): Quantitation of BDNF mRNA in human parietal cortex by competitive reverse transcription-polymerase chain reaction: decreased levels in Alzheimer’s disease. Brain Res Mol Brain Res. 2000 Mar 29;76(2):347-54. ↥

  29. Connor, Young, Yan, Faull, Synek, Dragunow (1997): Brain-derived neurotrophic factor is reduced in Alzheimer’s disease. Brain Res Mol Brain Res. 1997 Oct 3;49(1-2):71-81. ↥

  30. Narisawa-Saito, Wakabayashi, Tsuji, Takahashi, Nawa (1996): Regional specificity of alterations in NGF, BDNF and NT-3 levels in Alzheimer’s disease. Neuroreport. 1996 Nov 25;7(18):2925-8. ↥ ↥ ↥

  31. Zarrouki (2012): Die Wirkung des BDNF-Polymorphismus auf transkraniell induzierte Neuroplastizität, Dissertation ↥ ↥

  32. Duman, Monteggia (2006): A neurotrophic model for stress-related mood disorders. Biol Psychiatry. 2006 Jun 15;59(12):1116-27. ↥

  33. Ueyama, Kawai, Nemoto, Sekimoto, Toné, Senba (1997): Immobilization stress reduced the expression of neurotrophins and their receptors in the rat brain. eurosci Res. 1997 Jun;28(2):103-10. ↥

  34. Smith, Makino, Kvetnansky, Post (1995): Stress and glucocorticoids affect the expression of brain-derived neurotrophic factor and neurotrophin-3 mRNAs in the hippocampus. J Neurosci. 1995 Mar;15(3 Pt 1):1768-77. ↥

  35. Smith, Cizza (1996): Stress-induced changes in brain-derived neurotrophic factor expression are attenuated in aged Fischer 344/N rats. Neurobiol Aging. 1996 Nov-Dec;17(6):859-64. ↥

  36. Gourley, Kedves, Olausson, Taylor (2009): A history of corticosterone exposure regulates fear extinction and cortical NR2B, GluR2/3, and BDNF. Neuropsychopharmacology. 2009 Feb;34(3):707-16. doi: 10.1038/npp.2008.123. ↥

  37. Eisch, Bolaños, de Wit, Simonak, Pudiak, Barrot, Verhaagen, Nestler (2003): Brain-derived neurotrophic factor in the ventral midbrain-nucleus accumbens pathway: a role in depression. Biol Psychiatry. 2003 Nov 15;54(10):994-1005. ↥

  38. Berton, McClung, Dileone, Krishnan, Renthal, Russo, Graham, Tsankova, Bolanos, Rios, Monteggia, Self, Nestler (2006): Essential role of BDNF in the mesolimbic dopamine pathway in social defeat stress. Science. 2006 Feb 10;311(5762):864-8. ↥

  39. Krishnan, Han, Graham, Berton, Renthal, Russo, Laplant, Graham, Lutter, Lagace, Ghose, Reister, Tannous, Green, Neve, Chakravarty, Kumar, Eisch, Self, Lee, Tamminga, Cooper, Gershenfeld, Nestler (2007): Molecular adaptations underlying susceptibility and resistance to social defeat in brain reward regions. Cell. 2007 Oct 19;131(2):391-404. ↥

  40. Lin, Ter Horst, Wichmann, Bakker, Liu, Li, Westenbroek (2009): Sex differences in the effects of acute and chronic stress and recovery after long-term stress on stress-related brain regions of rats. Cereb Cortex. 2009 Sep;19(9):1978-89. doi: 10.1093/cercor/bhn225. ↥

  41. Shepard RD, Gouty S, Kassis H, Berenji A, Zhu W, Cox BM, Nugent FS (2018): Targeting histone deacetylation for recovery of maternal deprivation-induced changes in BDNF and AKAP150 expression in the VTA. Exp Neurol. 2018 Nov;309:160-168. doi: 10.1016/j.expneurol.2018.08.002. PMID: 30102916; PMCID: PMC6139260. ↥ ↥

  42. Fumagalli, Racagni, Colombo, Riva (2003): BDNF gene expression is reduced in the frontal cortex of dopamine transporter knockout mice. Mol Psychiatry. 2003 Nov;8(11):898-9. doi: 10.1038/sj.mp.4001370. PMID: 14593425. ↥

  43. Leo, Sukhanov, Zoratto, Illiano, Caffino, Sanna, Messa, Emanuele, Esposito, Dorofeikova, Budygin, Mus, Efimova, Niello, Espinoza, Sotnikova, Hoener, Laviola, Fumagalli, Adriani, Gainetdinov (2018): Pronounced Hyperactivity, Cognitive Dysfunctions, and BDNF Dysregulation in Dopamine Transporter Knock-out Rats. J Neurosci. 2018 Feb 21;38(8):1959-1972. doi: 10.1523/JNEUROSCI.1931-17.2018. PMID: 29348190; PMCID: PMC5824739. ↥ ↥ ↥ ↥ ↥ ↥ ↥ ↥

  44. Spires, Grote, Varshney, Cordery, van Dellen, Blakemore, Hannan (2004): Environmental enrichment rescues protein deficits in a mouse model of Huntington’s disease, indicating a possible disease mechanism. J Neurosci. 2004 Mar 3;24(9):2270-6. ↥

  45. Archer, Kostrzewa (2012): Physical exercise alleviates ADHD symptoms: regional deficits and development trajectory. Neurotox Res. 2012 Feb;21(2):195-209. doi: 10.1007/s12640-011-9260-0. ↥

  46. Neeper, Gómez-Pinilla, Choi, Cotman (1996): Physical activity increases mRNA for brain-derived neurotrophic factor and nerve growth factor in rat brain. Brain Res. 1996 Jul 8;726(1-2):49-56. ↥

  47. Oliff, Berchtold, Isackson, Cotman (1998): Exercise-induced regulation of brain-derived neurotrophic factor (BDNF) transcripts in the rat hippocampus. Brain Res Mol Brain Res. 1998 Oct 30;61(1-2):147-53. ↥

  48. Berchtold, Kesslak, Pike, Adlard, Cotman (2001): Estrogen and exercise interact to regulate brain-derived neurotrophic factor mRNA and protein expression in the hippocampus. Eur J Neurosci. 2001 Dec;14(12):1992-2002. ↥

  49. Lee, Duan, Long, Ingram, Mattson (2000): Dietary restriction increases the number of newly generated neural cells, and induces BDNF expression, in the dentate gyrus of rats. J Mol Neurosci. 2000 Oct;15(2):99-108. ↥

  50. Bova, Micheli, Qualadrucci, Zucconi (1989): BDNF and trkB mRNAs oscillate in rat brain during the light-dark cycle. Brain Res Mol Brain Res. 1998 Jun 15;57(2):321-4. ↥

  51. Berchtold, Oliff, Isackson, Cotman (1999): Hippocampal BDNF mRNA shows a diurnal regulation, primarily in the exon III transcript. Brain Res Mol Brain Res. 1999 Jul 23;71(1):11-22. ↥

  52. Pollock, Vernon, Forbes, Yan, Ma, Hsieh, Robichon, Frost, Johnson (2001): Effects of early visual experience and diurnal rhythms on BDNF mRNA and protein levels in the visual system, hippocampus, and cerebellum. J Neurosci. 2001 Jun 1;21(11):3923-31. ↥ ↥

  53. Liang, Walline, Earnest (1998): Circadian rhythm of brain-derived neurotrophic factor in the rat suprachiasmatic nucleus. Neurosci Lett. 1998 Feb 13;242(2):89-92. ↥

  54. Castrén, Zafra, Thoenen, Lindholm (1992): Light regulates expression of brain-derived neurotrophic factor mRNA in rat visual cortex. Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9444-8. ↥

  55. Cirelli, Tononi (2000) Differential Expression of Plasticity-Related Genes in Waking and Sleep and Their Regulation by the Noradrenergic System. Journal of Neuroscience 15 December 2000, 20 (24) 9187-9194; DOI: https://doi.org/10.1523/JNEUROSCI.20-24-09187.2000 ↥

  56. Rocamora, Welker, Pascual, Soriano (1996): Upregulation of BDNF mRNA expression in the barrel cortex of adult mice after sensory stimulation. J Neurosci. 1996 Jul 15;16(14):4411-9. ↥

  57. Nanda, Mack (2000): Seizures and sensory stimulation result in different patterns of brain derived neurotrophic factor protein expression in the barrel cortex and hippocampus. Brain Res Mol Brain Res. 2000 May 31;78(1-2):1-14. ↥

  58. Chen, Chiu, Chen, Hsu, Tzang (2018): Effects of taurine on striatal dopamine transporter expression and dopamine uptake in SHR rats; Behav Brain Res. 2018 Apr 22. pii: S0166-4328(18)30306-1. doi: 10.1016/j.bbr.2018.04.031. ↥

  59. Sulzer D, Cragg SJ, Rice ME (2016): Striatal dopamine neurotransmission: regulation of release and uptake. Basal Ganglia. 2016 Aug;6(3):123-148. doi: 10.1016/j.baga.2016.02.001. PMID: 27141430; PMCID: PMC4850498. REVIEW ↥ ↥

  60. Cordeira JW, Frank L, Sena-Esteves M, Pothos EN, Rios M (2010): Brain-derived neurotrophic factor regulates hedonic feeding by acting on the mesolimbic dopamine system. J Neurosci. 2010 Feb 17;30(7):2533-41. doi: 10.1523/JNEUROSCI.5768-09.2010. PMID: 20164338; PMCID: PMC2846779. ↥

  61. Bosse KE, Maina FK, Birbeck JA, France MM, Roberts JJ, Colombo ML, Mathews TA (2012): Aberrant striatal dopamine transmitter dynamics in brain-derived neurotrophic factor-deficient mice. J Neurochem. 2012 Feb;120(3):385-95. doi: 10.1111/j.1471-4159.2011.07531.x. PMID: 21988371; PMCID: PMC3385875. ↥

  62. Kramer ER, Liss B (2015): GDNF-Ret signaling in midbrain dopaminergic neurons and its implication for Parkinson disease. FEBS Lett. 2015 Dec 21;589(24 Pt A):3760-72. doi: 10.1016/j.febslet.2015.11.006. PMID: 26555190. REVIEW ↥

  63. Gash DM, Zhang Z, Cass WA, Ovadia A, Simmerman L, Martin D, Russell D, Collins F, Hoffer BJ, Gerhardt GA (1995): Morphological and functional effects of intranigrally administered GDNF in normal rhesus monkeys. J Comp Neurol. 1995 Dec 18;363(3):345-58. doi: 10.1002/cne.903630302. PMID: 8847404. ↥

  64. Salvatore MF, Zhang JL, Large DM, Wilson PE, Gash CR, Thomas TC, Haycock JW, Bing G, Stanford JA, Gash DM, Gerhardt GA (2004): Striatal GDNF administration increases tyrosine hydroxylase phosphorylation in the rat striatum and substantia nigra. J Neurochem. 2004 Jul;90(1):245-54. doi: 10.1111/j.1471-4159.2004.02496.x. PMID: 15198683. ↥

  65. Pothos EN, Davila V, Sulzer D (1998): Presynaptic recording of quanta from midbrain dopamine neurons and modulation of the quantal size. J Neurosci. 1998 Jun 1;18(11):4106-18. doi: 10.1523/JNEUROSCI.18-11-04106.1998. PMID: 9592091; PMCID: PMC6792796. ↥

  66. Sulzer D, Cragg SJ, Rice ME (2016): Striatal dopamine neurotransmission: regulation of release and uptake. Basal Ganglia. 2016 Aug;6(3):123-148. doi: 10.1016/j.baga.2016.02.001. PMID: 27141430; PMCID: PMC4850498. REVIEW ↥ ↥

  67. Cubero-Millán, Ruiz-Ramos, Molina-Carballo, Martínez-Serrano, Fernández-López, Machado-Casas, Tortosa-Pinto, Ruiz-López, Luna-Del-Castillo, Uberos, Muñoz-Hoyos (2016): BDNF concentrations and daily fluctuations differ among ADHD children and respond differently to methylphenidate with no relationship with depressive symptomatology. Psychopharmacology (Berl). 2017 Jan;234(2):267-279. doi: 10.1007/s00213-016-4460-1. n = 148 ↥

  68. Corominas-Roso M, Ramos-Quiroga JA, Ribases M, Sanchez-Mora C, Palomar G, Valero S, Bosch R, Casas M (2013): Decreased serum levels of brain-derived neurotrophic factor in adults with attention-deficit hyperactivity disorder. Int J Neuropsychopharmacol. 2013 Jul;16(6):1267-1275. doi: 10.1017/S1461145712001629. PMID: 23363778. n = 113 ↥

  69. Akay AP, Resmi H, Güney SA, Erkuran HÖ, Özyurt G, Sargin E, Topuzoglu A, Tufan AE (2018): Serum brain-derived neurotrophic factor levels in treatment-naïve boys with attention-deficit/hyperactivity disorder treated with methylphenidate: an 8-week, observational pretest-posttest study. Eur Child Adolesc Psychiatry. 2018 Jan;27(1):127-135. doi: 10.1007/s00787-017-1022-y. PMID: 28710695. n = 100 ↥ ↥

  70. El-Saied MM, Afify O, Abdelraouf ER, Oraby A, Hashish AF, Zeidan HM (2024): BDNF, proBDNF and proBDNF/BDNF ratio with electroencephalographic abnormalities in children with attention deficit hyperactivity disorder: Possible relations to cognition and severity. Int J Dev Neurosci. 2024 Aug;84(5):368-380. doi: 10.1002/jdn.10332. PMID: 38712701. ↥ ↥

  71. Sayyah H (2009): BDNF Plasma Level in ADHD Children: Correlation to Different Symptomatology. Curr. Psychiatry Egypt. 2009;16:284–294 n = 41 ↥ ↥ ↥

  72. Saadat F, Kosha M, Amiry A, Torabi G (2015): Brain-Derived Neurotrophic Factor as a Biomarker in Children with Attention Deficit-Hyperactivity Disorder. Journal of Krishna Institute of Medical Sciences (JKIMSU), 4(4). ↥

  73. Chang JP, Mondelli V, Satyanarayanan SK, Chiang YJ, Chen HT, Su KP, Pariante CM (2020): Cortisol, inflammatory biomarkers and neurotrophins in children and adolescents with attention deficit hyperactivity disorder (ADHD) in Taiwan. Brain Behav Immun. 2020 Aug;88:105-113. doi: 10.1016/j.bbi.2020.05.017. PMID: 32418647. n = 119 ↥

  74. Archer, Kostrzewa (2012): Physical exercise alleviates ADHD symptoms: regional deficits and development trajectory. Neurotox Res. 2012 Feb;21(2):195-209. doi: 10.1007/s12640-011-9260-0. REVIEW ↥

  75. Tsai SJ. Attention-deficit hyperactivity disorder may be associated with decreased central brain-derived neurotrophic factor activity: clinical and therapeutic implications. Med Hypotheses. 2007;68(4):896-9. doi: 10.1016/j.mehy.2006.06.025. PMID: 16919891. REVIEW ↥

  76. Gumus C, Yazici IP, Yazici KU, Ustundag B (2022): Increased Serum Brain-derived Neurotrophic Factor, Nerve Growth Factor, Glial-derived Neurotrophic Factor and Galanin Levels in Children with Attention Deficit Hyperactivity Disorder, and the Effect of 10 Weeks Methylphenidate Treatment. Clin Psychopharmacol Neurosci. 2022 Nov 30;20(4):635-648. doi: 10.9758/cpn.2022.20.4.635. PMID: 36263639; PMCID: PMC9606423. n = 118 ↥ ↥

  77. Taha H, Elsheshtawy E, Mohamed S I, Al-Azazzy O, Elsayed M, Ibrahim S A S (2017): Correlates of brain derived neurotrophic factor in children with attention deficit hyperactivity disorder: A case-control study. Egypt. J. Psychiatry, 38(3), 159-163. ↥

  78. Li H, Liu L, Tang Y, Ji N, Yang L, Qian Q, Wang Y (2014): Sex-specific association of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism and plasma BDNF with attention-deficit/hyperactivity disorder in a drug-naïve Han Chinese sample. Psychiatry Res. 2014 Jul 30;217(3):191-7. doi: 10.1016/j.psychres.2014.03.011. PMID: 24713358. n = 325 ↥

  79. Shim SH, Hwangbo Y, Kwon YJ, Jeong HY, Lee BH, Lee HJ, Kim YK (2008): Increased levels of plasma brain-derived neurotrophic factor (BDNF) in children with attention deficit-hyperactivity disorder (ADHD). Prog Neuropsychopharmacol Biol Psychiatry. 2008 Dec 12;32(8):1824-8. doi: 10.1016/j.pnpbp.2008.08.005. n = 148 ↥

  80. Demirci E, Gul MK, Sener EF, Onal MG, Dal F (2024): Assessment of BDNF and sialic acid levels in children with ADHD: Relation of chronotypes. Int J Dev Neurosci. 2024 Dec;84(8):857-866. doi: 10.1002/jdn.10376. PMID: 39308139. ↥

  81. El Ghamry R, El-Sheikh M, Abdel Meguid M, Nagib S, Aly El Gabry D (2021): Plasma brain-derived neurotrophic factor (BDNF) in Egyptian children with attention deficit hyperactivity disorder. Middle East Current Psychiatry, 28(1), 22. ↥

  82. Zhang J, Luo W, Li Q, Xu R, Wang Q, Huang Q (2018): Peripheral brain-derived neurotrophic factor in attention-deficit/hyperactivity disorder: A comprehensive systematic review and meta-analysis. J Affect Disord. 2018 Feb;227:298-304. doi: 10.1016/j.jad.2017.11.012. Epub 2017 Nov 6. PMID: 29132072. METASTUDY ↥

  83. Vogel, Bijlenga, Verduijn, Bron, Beekman, Kooij, Penninx (2017): Attention-deficit/hyperactivity disorder symptoms and stress-related biomarkers. Psychoneuroendocrinology. 2017 May;79:31-39. doi: 10.1016/j.psyneuen.2017.02.009. n = 2.307 ↥

  84. Yurteri, Şahin, Tufan (2019): Altered serum levels of vascular endothelial growth factor and glial-derived neurotrophic factor but not fibroblast growth factor-2 in treatment-naive children with attention deficit/hyperactivity disorder. Nord J Psychiatry. 2019 May – Jul;73(4-5):302-307. doi: 10.1080/08039488.2019.1625437. ↥ ↥

  85. Scassellati C, Zanardini R, Tiberti A, Pezzani M, Valenti V, Effedri P, Filippini E, Conte S, Ottolini A, Gennarelli M, Bocchio-Chiavetto L (2014): Serum brain-derived neurotrophic factor (BDNF) levels in attention deficit-hyperactivity disorder (ADHD). Eur Child Adolesc Psychiatry. 2014 Mar;23(3):173-7. doi: 10.1007/s00787-013-0447-1. PMID: 23812866. n = 90 ↥

  86. de Lucca MS, Pimentel MEO, Raimundo CKO, Henriques BD, Moreira TR, Cardoso SA, de Miranda DM (2023): Brain-derived neurotrophic factor (BDNF) levels in children and adolescents before and after stimulant use a systematic review and metanalysis. Prog Neuropsychopharmacol Biol Psychiatry. 2023 Jul 13;125:110761. doi: 10.1016/j.pnpbp.2023.110761. PMID: 37044279. METASTUDY ↥ ↥

  87. Huang W, Fateh AA, Zhao Y, Zeng H, Yang B, Fang D, Zhang L, Meng X, Hassan M, Wen F (2023): Effects of the SNAP-25 Mnll variant on hippocampal functional connectivity in children with attention deficit/hyperactivity disorder. Front Hum Neurosci. 2023 Aug 10;17:1219189. doi: 10.3389/fnhum.2023.1219189. PMID: 37635807; PMCID: PMC10447972. ↥

  88. Gerritsen L, Tendolkar I, Franke B, Vasquez AA, Kooijman S, Buitelaar J, Fernández G, Rijpkema M (2012): BDNF Val66Met genotype modulates the effect of childhood adversity on subgenual anterior cingulate cortex volume in healthy subjects. Mol Psychiatry. 2012 Jun;17(6):597-603. doi: 10.1038/mp.2011.51. PMID: 21577214. ↥

  89. Woelfer M, Li M, Colic L, Liebe T, Di X, Biswal B, Murrough J, Lessmann V, Brigadski T, Walter M (2020): Ketamine-induced changes in plasma brain-derived neurotrophic factor (BDNF) levels are associated with the resting-state functional connectivity of the prefrontal cortex. World J Biol Psychiatry. 2020 Nov;21(9):696-710. doi: 10.1080/15622975.2019.1679391. PMID: 31680600. RCT ↥

  90. Chan JP, Unger TJ, Byrnes J, Rios M (2006): Examination of behavioral deficits triggered by targeting Bdnf in fetal or postnatal brains of mice. Neuroscience. 2006 Sep 29;142(1):49-58. doi: 10.1016/j.neuroscience.2006.06.002. PMID: 16844311. ↥

  91. Rios M, Fan G, Fekete C, Kelly J, Bates B, Kuehn R, Lechan RM, Jaenisch R (2001): Conditional deletion of brain-derived neurotrophic factor in the postnatal brain leads to obesity and hyperactivity. Mol Endocrinol. 2001 Oct;15(10):1748-57. doi: 10.1210/mend.15.10.0706. PMID: 11579207. ↥ ↥

  92. Tsai SJ. Attention-deficit hyperactivity disorder may be associated with decreased central brain-derived neurotrophic factor activity: clinical and therapeutic implications. Med Hypotheses. 2007;68(4):896-9. doi: 10.1016/j.mehy.2006.06.025. PMID: 16919891. ↥

  93. Kernie SG, Liebl DJ, Parada LF (2000): BDNF regulates eating behavior and locomotor activity in mice. EMBO J. 2000 Mar 15;19(6):1290-300. doi: 10.1093/emboj/19.6.1290. PMID: 10716929; PMCID: PMC305670. ↥

  94. Amiri A, Torabi Parizi G, Kousha M, Saadat F, Modabbernia MJ, Najafi K, Atrkar Roushan Z (2013): Changes in plasma Brain-derived neurotrophic factor (BDNF) levels induced by methylphenidate in children with Attention deficit-hyperactivity disorder (ADHD). Prog Neuropsychopharmacol Biol Psychiatry. 2013 Dec 2;47:20-4. doi: 10.1016/j.pnpbp.2013.07.018. PMID: 23933054. n = 28 ↥

  95. Roeding, Perna, Cummins, Peterson, Palmatier, Brown (2014): Sex differences in adolescent methylphenidate sensitization: effects on glial cell-derived neurotrophic factor and brain-derived neurotrophic factor. Behav Brain Res. 2014 Oct 15;273:139-43. doi: 10.1016/j.bbr.2014.07.014. ↥ ↥

  96. Fumagalli, Cattaneo, Caffino, Ibba, Racagni, Carboni, Gennarelli, Riva (2010): Sub-chronic exposure to atomoxetine up-regulates BDNF expression and signalling in the brain of adolescent spontaneously hypertensive rats: comparison with methylphenidate. Pharmacol Res. 2010 Dec;62(6):523-9. doi: 10.1016/j.phrs.2010.07.009. ↥

  97. Ramon-Duaso, Gener, Consegal, Fernández-Avilés, Gallego, Castarlenas, Swanson, de la Torre, Maldonado, Puig, Robledo (2019): Methylphenidate Attenuates the Cognitive and Mood Alterations Observed in Mbnl2 Knockout Mice and Reduces Microglia Overexpression. Cereb Cortex. 2019 Jul 5;29(7):2978-2997. doi: 10.1093/cercor/bhy164. ↥

  98. Warren, Iñiguez, Alcantara, Wright, Parise, Weakley, Bolaños-Guzmán (2011): Juvenile administration of concomitant methylphenidate and fluoxetine alters behavioral reactivity to reward- and mood-related stimuli and disrupts ventral tegmental area gene expression in adulthood. J Neurosci. 2011 Jul 13;31(28):10347-58. doi: 10.1523/JNEUROSCI.1470-11.2011. ↥

  99. Simchon Tenenbaum, Weizman, Rehavi (2015): The Impact of Chronic Early Administration of Psychostimulants on Brain Expression of BDNF and Other Neuroplasticity-Relevant Proteins. J Mol Neurosci. 2015 Oct;57(2):231-42. doi: 10.1007/s12031-015-0611-9. ↥

  100. Cubero-Millán, Ruiz-Ramos, Molina-Carballo, Martínez-Serrano, Fernández-López, Machado-Casas, Tortosa-Pinto, Ruiz-López, Luna-Del-Castillo, Uberos, Muñoz-Hoyos (2016): BDNF concentrations and daily fluctuations differ among ADHD children and respond differently to methylphenidate with no relationship with depressive symptomatology. Psychopharmacology (Berl). 2017 Jan;234(2):267-279. doi: 10.1007/s00213-016-4460-1. ↥

  101. Brown, Hughes, Hughes, Sheppard, Perna, Ragsdale, Roeding, Pond (2012): Sex and dose-related differences in methylphenidate adolescent locomotor sensitization and effects on brain-derived neurotrophic factor. J Psychopharmacol. 2012 Nov;26(11):1480-8. doi: 10.1177/0269881112454227. ↥

  102. Chase, Carrey, Soo, Wilkinson (2006): Methylphenidate regulates activity regulated cytoskeletal associated but not brain-derived neurotrophic factor gene expression in the developing rat striatum. Neuroscience. 2007 Feb 9;144(3):969-84. ↥

  103. Andersen, Sonntag (2014): Juvenile methylphenidate reduces prefrontal cortex plasticity via D3 receptor and BDNF in adulthood. Front Synaptic Neurosci. 2014 Jan 21;6:1. doi: 10.3389/fnsyn.2014.00001. eCollection 2014. ↥

  104. Wetzell, Muller, Cobuzzi, Hurwitz, DeCicco-Skinner, Riley (2014): Effect of age on methylphenidate-induced conditioned taste avoidance and related BDNF/TrkB signaling in the insular cortex of the rat. Psychopharmacology (Berl). 2014 Apr;231(8):1493-501. doi: 10.1007/s00213-014-3500-y. ↥

  105. Fumagalli F, Cattaneo A, Caffino L, Ibba M, Racagni G, Carboni E, Gennarelli M, Riva MA (2010): Sub-chronic exposure to atomoxetine up-regulates BDNF expression and signalling in the brain of adolescent spontaneously hypertensive rats: comparison with methylphenidate. Pharmacol Res. 2010 Dec;62(6):523-9. doi: 10.1016/j.phrs.2010.07.009. PMID: 20691787. ↥

  106. Ramos-Quiroga JA, Corominas-Roso M, Palomar G, Gomez-Barros N, Ribases M, Sanchez-Mora C, Bosch R, Nogueira M, Corrales M, Valero S, Casas M. Changes in the serum levels of brain-derived neurotrophic factor in adults with attention deficit hyperactivity disorder after treatment with atomoxetine. Psychopharmacology (Berl). 2014 Apr;231(7):1389-95. doi: 10.1007/s00213-013-3343-y. PMID: 24202115. n = 35 ↥

  107. Lee, Lee, Kim, Yan, Park, Kwon, Park, Ahn, Cho, Won, Kim (2012): Effects of ADHD therapeutic agents, methylphenidate and atomoxetine, on hippocampal neurogenesis in the adolescent mouse dentate gyrus. Neurosci Lett. 2012 Aug 30;524(2):84-8. doi: 10.1016/j.neulet.2012.07.029. ↥

  108. Torun, Güney, Aral, Büyüktaşkin, Tunca, Taner, İşeri (2019): Determination of Serum Vascular Endothelial Growth Factor Levels in Attention Deficit Hyperactivity Disorder: A Case Control Study. Clin Psychopharmacol Neurosci. 2019 Nov 20;17(4):517-522. doi: 10.9758/cpn.2019.17.4.517. n = 87 ↥

  109. Ertürk E, Işık Ü, Şirin FB. Analysis of Serum VEGF, IGF-1, and HIF-1α Levels in ADHD. J Atten Disord. 2023 Sep 13:10870547231197211. doi: 10.1177/10870547231197211. PMID: 37700676. n = 80 ↥

  110. Kim J, Lee S, Choi BR, Yang H, Hwang Y, Park JH, LaFerla FM, Han JS, Lee KW, Kim J (2017): Sulforaphane epigenetically enhances neuronal BDNF expression and TrkB signaling pathways. Mol Nutr Food Res. 2017 Feb;61(2). doi: 10.1002/mnfr.201600194. PMID: 27735126. ↥

  111. Borodinova A A, Salozhin S V (2017): Differences in the Biological Functions of BDNF and proBDNF in the Central Nervous System. Neuroscience and Behavioral Physiology, 47(3), 251-265. ↥

  112. Chen NC, Chuang YC, Huang CW, Lui CC, Lee CC, Hsu SW, Lin PH, Lu YT, Chang YT, Hsu CW, Chang CC (2016): Interictal serum brain-derived neurotrophic factor level reflects white matter integrity, epilepsy severity, and cognitive dysfunction in chronic temporal lobe epilepsy. Epilepsy Behav. 2016 Jun;59:147-54. doi: 10.1016/j.yebeh.2016.02.029. PMID: 27152461. ↥

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