Alzheimer drugs:

Alzheimer's disease (AD), is one form
of dementia that gradually gets worse
over time. It affects memory, thinking,
and behavior.

Memory impairment, as well as
problems with language, decision-
making ability, judgment, and
personality, are necessary features for
the diagnosis.

Inhalation of insulin through the nose
twice a day appears to slow down and,
in some cases, reverse symptoms of
memory loss in people with early signs
of Alzheimer's disease, a new study

The results were published in the
journal Archives of Neurology Iin
September 2011.

The study, led by Suzanne Craft, a
professor of psychiatry and behavioral
sciences at the University of
Washington. She led the research
team at the Veterans Affairs Puget
Sound Health Care System and the
university's medical school in Seattle.

The study involved 104 patients with
mild cognitive decline or mild to
moderate case of Alzheimer's.

Study participants were randomly
assigned to one of three groups. In
first group, 36 participants got a
moderate dose of insulin sprayed daily
into their nose. In second group, 36
patients got a higher dose daily. In
third group, 30 participants got a
placebo daily for four months.

After four months, the group that got
the moderate insulin dose showed
improvements in delayed story recall
compared with the placebo group.
There was no improvement in the
group that got the high dose compared
with the placebo group.

Eli  Lilly announced  that it was ending
its large clinical trials of the drug
semagacestat,  and researchers are

Beyond the setback for Lilly, the study
raises questions about a leading
hypothesis of the cause of Alzheimer’s
and how to treat it. The idea, known as
the amyloid hypothesis, says the
disease occurs when a toxic protein,
beta amyloid, accumulates in the brain.
The idea is that if beta amyloid levels
are reduced, the disease might be
slowed, halted or even prevented if
treatment starts early enough.
The Lilly drug, like most of the more
than 100 Alzheimer’s drugs under
development, blocks an enzyme,
gamma secretase, needed to make
beta amyloid. It was among the first
shown to broach the blood-brain
barrier and reduce levels of beta
amyloid in the brain. And, company
studies showed, it did reduce amyloid

It was not just that the drug, made by
Eli Lilly, did not work — maybe that
could be explained by saying the
patients’ illness was too far advanced
when they received it. It was that the
drug actually made them worse, the
company said. And the larger the dose
they took, the worse were patients’
symptoms of memory loss and inability
to care for themselves. Not only that,
the drug also increased the risk of skin

CPHPC by Pentraxin Therapeutics and
GlaxoSmithKline, removes a protein
SAP (serum  amyloid P component)
from the blood and brains of patients;


Bapineuzumab by J&J, Pfizer and Elan
Corp in development;

Razadyne by J&J;

Bristol-Myers Squibb Co. is also
working on a gamma secretase
inhibitor in early human testing;

Eisai Co.’s
best-selling Aricept;

Novartis AG’s Exelon;

New theory of Alzheimer's
explains drug failures

Brain plaques, long considered
the chief killer of brain cells and
the cause of Alzheimer's disease,
may actually play a protective role
under a new theory that is
changing the way researchers
think about the disease.

Instead of sticky plaques, free-
floating bits of a toxic protein
called amyloid beta may be what's
killing off brain cells in Alzheimer's
patients, U.S. researchers say.

If the theory is right, then drugs
that target plaque, including
bapineuzumab -- being developed
by Pfizer, Johnson & Johnson and
Elan -- may be aiming at the wrong
target, they say.


Alzheimer’s Isn’t Up to the
First, about the diagnostic tests: A
PET scan detects clumps of a
deformed protein called amyloid
beta, commonly known as plaques.
The presence of these plaques
has been a gold standard of
Alzheimer’s pathology since 1906,
when Dr. Alois Alzheimer first
identified them in a patient.

However, we now know that
roughly one-third of all elderly
adults have such plaques in their
brains yet function normally. And
eleven clinical trials, recently
made public by a group of drug
companies, that were aimed at
reducing these plaques in
Alzheimer’s patients all failed to
show cognitive improvement,
even when the brains were
cleared of plaques.


For more than two decades, the prevailing
plan of attack for researchers and drug
companies has been to find a way to
remove sticky clumps of a protein called
amyloid beta from the brain.

But several recent studies in mice and rats
now suggest that floating pieces of amyloid
beta called oligomers are the real bad
actors in Alzheimer's disease.