New Alzheimer Drugs on the Horizon!

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New Alzheimer Drugs on the Horizon
Here's breaking news for those affected by
Alzheimer's! Four new drugs are being tested that
work in a unique manner, unlike other current
medicines. Below are the exciting details on
these up-and-coming drugs.
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Anatomy OfALZHEIMER'S
The entities responsible for Alzheimer's disease
are plaques and tangles. Plaques are protein
fragments called amyloid that accumulate between
brain cells. Tangles are twisted protein fibers
that form inside the cells. These protein clumps
block communication and disrupts cellular
processes. To see a diagram of plaques and
tangles, go to http//www.savethesynapse.com/wp/wp
-content/uploads/2011/11/plaque.jpg.
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Plaques AndTangles
The development of plaques and tangles is a
normal aspect of aging. However, when the process
becomes widespread, it significantly impairs
mental function. An Alzheimer's brain exhibits
protein clumps in a characteristic pattern. The
abnormality originates in brain regions involved
in memory and then spreads to other areas.
Eventually, brain cells die, causing the signs
and symptoms of Alzheimer's disease (AD).
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ANTIBODY
DEFENSE
Preliminary testing of a new drug has shown it to
reduce the decline in memory and thinking skills
in the early stages of AD. The medication is
called Adu can mab. It works like an antibody,
attacking plaques. An antibody is a protein that
identifies and neutralizes alien invaders.
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LANDMARK S T U D Y
The Adu can mab investigation was initiated in
the summer of 2012. It involved 166 adults in the
early stages of AD. All the subjects had evidence
of plaque build-up. Patients were divided into
four groups, receiving either low, medium, or
high drug doses or a placebo. In March 2015, an
interim analysis of the first data was reported.
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F I N D
I N G S
The outcome at one year was monumental! The
higher the drug dose, the fewer patients erred on
clinical tests of memory and thinking. Aducanumab
subjects demonstrated 70 percent less mental
decline than placebo patients! Study participants
also underwent brain imaging, with radioactive
tracers used to identify brain plaques.
Aducanumab reduced plaque deposition in six brain
regions. In placebo subjects, protein clumps
remained unchanged. Low doses of the drug didnt
impact brain plaque. However, both medium and
high doses noticeably lowered plaque levels.
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SIDE EFFECT
Most of the study participants tolerated the
medication well. Brain scans of those on the
higher doses revealed some brain swelling.
Although the inflammation did not produce
symptoms, researchers are concerned about future
problems. Brain swelling was most pronounced in
patients carrying the gene for AD. Headaches
arose in 22 percent of patients given the drug,
appearing to be dose-related. The headaches
quickly resolved.
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FORECAST
Aducanumab is a pioneer in the fight against AD.
To date, there have been no other medications
that destroy brain plaques. Current drugs
decelerate the disease process temporarily but
are unable to halt completely its progression.
Aducanumab significantly retards plaque
formation. The drug is the brainchild of the
Biogen company, based in Massachusetts. Clinical
testing is in the final Phase 3 stage. This
segment of evaluation involves a large study
group of 1,350 patients over five years. Thorough
testing on a broad scale is required before the
drug can be marketed. Analysts expect that within
three years, the data will indicate whether Adu
can mab is the "Goldilocks" drug, the "just
right" formulation that will resolve AD.
Researchers are optimistic regarding the drug's
potential.
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THE
JOINING CRUSADE
Also in the testing phase are three other
medications, solanezumab, gantenerumab, and
crenezumab. Solanezumab - The drug manufacturer
Eli Lilly is testing this drug. Solanezumab is
also designed to attack brain plaques. The drug
appears to help mild AD. Gantenerumab - Roche
Pharmaceuticals has produced this anti-amyloid
drug. Data from spinal fluid tests and brain
scans are promising. Crenezumab - The Genentech
company has formulated this drug, targeted to
mild AD. Research is now in the Phase 3 stage.
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CURRENT DRUG MECHANISMS

• Current drugs work by relieving some AD symptoms.
  However, they do not address the cause of AD or
  delay its advancement. The FDA has approved two
  classes of drugs for the treatment of Alzheimer's
  disease. Until alternative medications are
  marketed, these are the two options available
• Cholinesterase Inhibitors
• Memantine
•  
• Each drug acts on a different brain region, so
  physicians sometimes prescribe both
  simultaneously. The medications are also designed
  for specific stages of AD - mild, moderate, and
  severe. These delineations are based on mental
  function test scores, measuring memory, thinking,
  reasoning, and awareness of time and place.

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CHOLINESTERASE INHIBITORS (CIs)
Plaques and tangles decrease levels of
acetylcholine, a chemical involved in memory,
alertness, thought, and judgment. CIs prevent the
breakdown of acetylcholine. Unfortunately, the
drugs are unable to stop disease progression.
Although they make acetylcholine more available,
brain cells continue to die. Therefore, the drugs
lose their effectiveness over time. There are
three FDA-approved CIs. In clinical studies, all
of them work equally well. However, individual
response varies regarding drug performance and
side effects. Symptoms include nausea, vomiting,
and diarrhea. Side effects are reduced when a
drug is started at a low dose and gradually
increased. Taking a CI with food also helps
minimize discomfort. The three CIs commonly
prescribed are Aricept, Razadyne, and Exelon.
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ARICEPT
Aricept - treats all stages of AD. It is taken
once a day in pill form. It is typically
well-tolerated, with side effects occurring in
only 20 percent of people with AD. Razadyne -
targets mild to moderate AD and is available as a
pill and syrup. It has been shown to slow
cognitive decline for up to three years. Exelon -
for mild to moderate AD, available as a skin
patch, pill, and syrup. It is comparable to
Aricept regarding efficacy but may cause more
gastrointestinal side effects.
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Memantine
Under the brand name Namenda, this medication
addresses moderate to severe AD. It has a
different treatment mechanism. It regulates
glutamate, a chemical involved in learning and
memory. Namenda is formulated as a pill and
syrup. Common side effects include a headache,
confusion, dizziness, and agitation.
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STAY TUNED!
Alzforum has the most current information
available on the four drugs. The website's August
2015 report summarizes the outcome of this year's
Alzheimer's Association International
Conference. Aducanumab - Researchers are trying
to determine the optimal dose of Adu can mab.
Three dosages have undergone trial, 3 mg, 6 mg,
and 10 mg, with none of them quite hitting the
mark. The 10 mg dose is most effective against
plaques but causes brain swelling. It was thought
that a 6-mg dose would be ideal, but it has not
delivered the desired outcome. Phase 3 of the
study will continue exploring drug dosages versus
side effects.
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Solanezumab - Research on solanezumab has shown a
34 percent decline in disease progression! Phase
3 for solanezumab will be complete by October
2016. Gantenerumab - Study of Gantenerumab has
yielded gains in biomarker data. A biomarker is a
biological indicator of disease. The trial has
promoted a greater understanding of the nature of
AD. Patients with severe AD have had a positive
response at a high dose, with a 5 percent
reduction in brain plaque. Roche is moving into
Phase 3, to assess further the effects of high
doses. Crenezumab - This medication does not
cause brain swelling, enabling use at higher
doses. The drug shows promise as a treatment for
mild AD. It's also being tested as a preventative
drug, the first of its kind! Study results will
be forthcoming in 2020.
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EYES ON THE PRIZE
Aducanumab is the first drug to exhibit a dual
effect on both plaque destruction and cognitive
decline. Conclusive data is three years away. The
outcome of solanezumab will be evident one year
from now. Results of gantenerumab and crenezumab
will follow. As research efforts get closer to a
cure for AD, we can be grateful for the diligence
of scientists. With their continued perseverance,
we can look forward to the day when AD is a faded
memory.
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SOURCES
  1. https//www.alzinfo.org/articles/diagnosis/ex
perimental-alzheimers-drug-aducanumab-slows-cognit
ive-decline-in-early-trials/   2.
http//www.alzforum.org/therapeutics/aducanumab  
3. http//www.alzforum.org/therapeutics/crenezumab
-0   4. http//www.alzforum.org/news/conference-co
verage/aducanumab-solanezumab-gantenerumab-data-li
ft-crenezumab-well   5. http//www.mayoclinic.org/
diseases-conditions/alzheimers-disease/in-depth/al
zheimers/art-20048103   6. http//blogs.discoverma
gazine.com/d-brief/2015/03/20/drug-alzheimers-dise
ase/.VkN64-Lw9uY
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