7,8-Dihydroxyflavone’s Multiple Neurological Benefits: Preventing Synaptic Loss and Memory Deficits


7,8-Dihydroxyflavone (7,8-DHF)

7,8-Dihydroxyflavone (7,8-DHF) is a naturally-occurring flavone found in:

  • Godmania aesculifolia
  • Tridax procumbens
  • Primula tree leaves

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Figure 1.  7,8-Dihydroxyflavone molecule  (Source)

Flavones are a class of flavonoids which are a class of plant secondary metabolites.

Natural flavones include:

  • Apigenin (4′,5,7-trihydroxyflavone)
  • Luteolin (3′,4′,5,7-tetrahydroxyflavone)
  • Tangeritin (4′,5,6,7,8-pentamethoxyflavone)
  • Chrysin (5,7-hydroxyflavone)
  • 6-hydroxyflavone
  • Baicalein (5,6,7-trihydroxyflavone)
  • Scutellarein (5,6,7,4′-tetrahydroxyflavone)
  • Wogonin (5,7-dihydroxy-8-methoxyflavone)

Synthetic flavones include:

  • Diosmin
  • Flavoxate
  • 7,8-dihydroxyflavone (7,8-DHF)

Neurological Benefits from 7,8-Dihydroxyflavone (7,8-DHF)

7,8-Dihydroxyflavone (7,8-DHF) has been determined and studied to be a potent and selective agonist of the TrkB receptor, which is the main signaling receptor of brain-derived neurotrophic factor (BDNF). It is able to penetrate the blood-brain-barrier after oral consumption.

7,8-DHF has been very therapeutically efficient in various central nervous system disorders including:

  • Depression [1]
  • Alzheimer’s disease [2]
  • Schizophrenia [3]
  • Parkinson’s disease [4]
  • Huntington’s disease [5]
  • Amyotrophic lateral sclerosis [6]
  • Traumatic brain injury [7]
  • Cerebral ischemia [8]

7,8-Dihydroxyflavone Prevents Synaptic Loss and Memory Deficits

A study from February 2014 in the Journal Neuropsychopharmacology identified 7,8-dihydroxyflavone (7,8-DHF) as a novel oral bioactive therapeutic agent for treating Alzheimer’s disease (AD). [9]

A synapse is a structure that permits a neuron (or nerve cell) to pass an electrical or chemical signal to another neuron.  Synapses are essential to neuronal function: neurons are cells that are specialized to pass signals to individual target cells, and synapses are the means by which they do so. At a synapse, the plasma membrane of the signal-passing neuron (the presynapticneuron) comes into close apposition with the membrane of the target (postsynaptic) cell. [10]

The loss of synapes’ and synaptic dysfunction in Alzheimer’s disease is correlated with deficits in brain-derived neurotrophic factor/tropomyosin-receptor-kinase B (TrkB) signaling.     

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Figure 2.  Synapse diagram  (Source)

In this study, the researchers tested the effect of 7,8-DHF on synaptic function in an AD model both in vitro and in vivo.

They found that 7,8-DHF:

  • protected primary neurons from amyloid-beta induced toxicity
  • promoted dendrite branching and synaptogenesis (growth of new synapses)
  • prevented amyloid-beta deposition
  • inhibited the loss of hippocampal synapses
  • restored synapse number
  • restored synaptic plasticity
  • prevented memory deficits