Dad’s diagnosis of Alzheimer’s stayed
hidden from everyone until I took over the medical administration of my parents
in 2015. Once I found out, there was a deafening silence from most of the
people I know even though virtually all of them would add, “My _____ had
Alzheimer’s…” But there was little help, little beyond people sadly shaking
heads. Or horror stories. Lots of those. Even the ones who knew about the
disease seemed to have received a gag order from some Central Alzheimer’s
Command and did little more than mumble about the experience. Not one to shut
up for any known reason, I started this part of my blog…
I’ll also be
trying to keep up with current research in Alzheimer’s treatments as well as
research into understanding exactly what the diseases does…and I’ll be looking
HARD for research on Alzheimer’s prevention – as that one has some real
importance for me and my siblings.
Today, I’ve found
some hopeful research on “curing” the disease. Mind you, it’s ONLY in the
mouse-testing phase, but given the number of people suffering from it, it would
seem to me that finding a way to prevent Alzheimer’s from occurring in the
first place would be high on SOMEONE’S research list.
Here’s the actual,
untranslated abstract (sort of like the summaries we had to do in middle school
about the books we read):
“Type 2 diabetes
mellitus (T2DM) is a risk factor for Alzheimer disease (AD). Previous studies
have shown that the incretin hormones glucagon-like peptide-1 (GLP-1) and
glucose-dependent insulinotropic polypeptide (GIP) that have anti-diabetic
properties show very promising effects in animal models of AD. Glucagon (Gcg)
is a hormone and growth-factor, and the Gcg receptor is expressed in the brain.
Here we test the effects of a triple receptor agonist (TA), which activates GLP-1,
GIP and glucagon receptors at the same time. In the present study, the effects
of the TA were evaluated in the APP/PS1 transgenic mouse model of AD. The TA
was injected once-daily (10 nmol/kg
i.p.) for two months. The results showed that treatment with TA significantly reversed the memory deficit in the APP/PS1
mice in a spatial water maze test. Moreover, the drug reduced levels of the
mitochondrial pro-apoptotic signaling molecule BAX, increased the
anti-apoptotic signaling molecule Bcl-2 and enhanced the levels of BDNF, a key
growth factor that protects synaptic function. Levels of synaptophysin were
enhanced, demonstrating protection from synaptic loss that is observed in AD.
Neurogenesis in the dentate gyrus was furthermore enhanced as shown in the increase
of doublecortin positive cells. Furthermore, TA treatment reduced the total
amount of β-amyloid, reduced neuroinflammation (activated microglia and
astrocytes), and oxidative stress in the cortex and hippocampus. Thus,
these findings show that novel TAs are a promising lead for the design of
future treatment strategies in AD.”
Like I used to do for
my wife’s breast cancer diagnosis and treatments, I’m going to make an attempt
to translate this. [To lend a little bit of credibility: I have a BS in Biology
and an MS in School Counseling. I have been a science geek since I was a
teenager, I love language, and I read and understand technical papers in both
fields. Science is full of jargon – but all jargon is, is an attempt to
communicate something as precisely as possible. You can probably find someone
else to translate for you, but they’d need more schooling than I’ve had…]
The abstract
begins by saying that people who are Type 2 diabetic (This means that they started
having insulin problems AFTER adolescence. Type 1 diabetics were called “juvenile
onset” at one time) have a higher risk of getting Alzheimer’s. It’s not a
guarantee (and my dad wasn’t diabetic), but there’s an increased risk there.
The researchers made
a “cocktail” of three different hormones that would lock into the brain
Research has shown
that two hormones that prevent people from becoming diabetic, ALSO appears to
protect people from developing Alzheimer’s. In the abstract, they name the
hormones, then abbreviate them, then continue to use LOTS of abbreviations (for
example, AD = Alzheimer’s Disease).
One of the
hormones contributes to growth in the human body. When the hormone travels to the
brain, there is a SPECIFIC site that it can hook into that is there; the
hormone can then signal the brain to grow more nerve cells that connect you to
your memories. The other two are the ones that protect the body from becoming
diabetic.
The researchers
injected a mixture of the hormone and diabetes protectors into mice every day
for two months. At the end of that period, a NUMBER of really good things had
happened!
First of all, the
treatment reversed memory loss! Moreover, the drug reduced the molecule that makes
a brain cell commit suicide and increased the amounts of molecules that both stop
the brain cell suicide and created TWO chemicals that stimulates growth and a
chemical that protects the nerves from attack by the molecule that starts the cell-suicide
process. It also acts on a part of the
brain called the “hippocampus” (I know, sounds like a place where zoo animals
go to school). It causes the growth of new nerves in a place called the “dentate
gyrus” (NOT someone who meditates on dentures), a place the guides the “formation
of new episodic memories, the spontaneous exploration of novel environments,
and other functions.” The injections reduced the amount of brain plaque that
has become associated with Alzheimer’s, and finally made the swelling in the
lining of the nerves go down.
All-in-all, the
research delivered a lot of what researchers are looking for. HOWEVER – this is
at the “injecting mice stage”. It’s a long, long way away from the “Hey, Doc!
Can I get me a set of those daily injections so I can get my memory back?” In
other words, this research won’t lead to a competitor for PREVAGEN (a miracle drug
(ABSOLUTELY NOT BEING SERIOUS HERE!!!). It’s years from being a real, clinical
treatment.
Then again, it’s
way better than the bad news we’ve been feasting on since the first attempt to
deal with the beta-amyloid plaques and Tau protein tangles the first Alzheimer’s
drug tried to attack in 1987…three decades ago.
I’m not going to
hold my breath. As with any research on finding a cure for any disease or
condition, much remains to be seen.
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