Here’s the study itself, it’s a little neurobiology heavy

β-Amyloid inhibits E-S potentiation through suppression of cannabinoid receptor 1-dependent synaptic disinhibition.

It has been widely reported that β-amyloid peptide (Aβ) blocks long-term potentiation (LTP) of hippocampal synapses. Here, we show evidence that Aβ more potently blocks the potentiation of excitatory postsynaptic potential (EPSP)-spike coupling (E-S potentiation). This occurs, not by direct effect on excitatory synapses or postsynaptic neurons, but rather through an indirect mechanism: reduction of endocannabinoid-mediated peritetanic disinhibition. During high-frequency (tetanic) stimulation, somatic synaptic inhibition is suppressed by endocannabinoids. We find that Aβ prevents this endocannabinoid-mediated disinhibition, thus leaving synaptic inhibition more intact during tetanic stimulation. This intact inhibition opposes the normal depolarization of hippocampal pyramidal neurons that occurs during tetanus, thus opposing the induction of synaptic plasticity. Thus, a pathway through which Aβ can act to modulate neural activity is identified, relevant to learning and memory and how it may mediate aspects of the cognitive decline seen in Alzheimer’s disease.

So basically from my layman’s interpretation: Synaptic inhibition, which means the synapse’s actions are blocked, is prevented by the endocannabinoids that occur naturally in our body. However, B-amyloid supresses the effects of what the endocannabinoids are doing – meaning that this synapse inhibition does occur.

For example, if you were a taxi driver for 20 years, your hippocamus would be larger than the general populations because that area of the brain deals with spatial skills and you would be using those skills everyday. Reducing plasticity is bad 🙁

My science lesson for today  :weinerwiggle: