The Unexpected Role of Nav1.6
Channels in Alzheimer's Disease
Did
you know there was a link between Nav channels
and amyloid beta (Aβ) in Alzheimer’s disease (AD)? In some exciting research, a
term has uncovered a crucial link between Nav1.6 and
the hyperexcitability of neurons in AD. Not only does this give new insight
into the role of Nav channels, but opens
up a promising avenue for potential therapeutics to counteract the early
stages of AD.
How
does Aβ relate to NaV1.6?
In
the search for answers, researchers turned their attention to voltage-gated
sodium channels, which are essential for regulating neuronal excitability.
These channels have been implicated in the hyperactivity of hippocampal neurons
in AD and the increased incidence of seizures. The team embarked on a journey,
using primary hippocampal neurons exposed to amyloid-β1–42 (Aβ1–42) oligomers,
a hallmark of AD, to unravel the mysteries of neuronal hyperexcitability. The
team relied on two different in vitro models to recapitulate amyloid pathology:
primary cultures of hippocampal neurons from mice treated with syn-thetic
Aβ1–42 oligomers for 24 hours, and primary cultures of hippocampal neurons from
Tg2576 mice, which endogenously produce Aβ1–42 peptides that accumulate over
time in culture. They also used the sodium channel blocker Tetrodotoxin
citrate (TTX) (#T-550) to block endogenous NaV
currents.
Read more…
Navigating
NaV Channels
To
help you fully explore the role of NaV channels,
here are helpful reagents.
Antibodies
and Controls
Pharmacological Tools
