Hospital Pharmacy - December 2017 - 737

735642
research-article2017

HPXXXX10.1177/0018578717735642Hospital PharmacyOrf and Walker

Pharmaceutical Pipeline Update

BACE Inhibitors and Tau Protein
Targeting Drugs in Prevention of
Alzheimer's Disease

Hospital Pharmacy
2017, Vol. 52(11) 737-739
© The Author(s) 2017
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https://doi.org/10.1177/0018578717735642
DOI: 10.1177/0018578717735642
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Jonathan Orf1 and Scot Walker2

Abstract
Alzheimer's disease (AD) is a common disease in the United States with almost 10% of people older than 65 suffering from
the disease. A few drugs provide some improvement in mental function in mild-to-moderate disease, but no treatments are
available to prevent the development of AD. Two new classes of drugs being investigated for the treatment or prevention of
AD include drugs to decrease beta amyloid accumulation and Tau protein aggregation inhibitors. After disappointing results
for treatment of AD, both classes are being tested in prevention trials.
Keywords
investigational drugs, formulary management/P&T, neurology

Epidemiology
Alzheimer's disease (AD) is the sixth leading cause of death in
the United States.1 Almost 10% of people aged 65 or older suffer from AD; they are not the only ones suffering. Caregivers to
people with the disease provided 18.2 billion hours of unpaid
service in 2016 alone. Predictions estimate that in 2017, AD
and other forms of dementia will cost the United States up to
$259 billion, making it the disease with the highest cost.2

Current Treatment
Currently, no treatment is available to prevent the development of AD. Instead, there are a few treatment options to
help reduce symptoms in patients with mild-to-moderate
forms of AD. Symptoms associated with disease progression
include loss of memory, loss of cognitive function, and loss
of judgment or the ability to solve problems. Cholinesterase
inhibitors including donepezil, galantamine, and rivastigmine help by inhibiting the breakdown of acetylcholine at
the synaptic cleft in turn increasing neuronal function and
reducing symptoms. Memantine, an N-methyl-d-aspartate
(NMDA) antagonist, has also been shown to improve mental
status scores with minimal risk of side effects in patients with
moderate-to-severe AD.3

buildup of beta amyloid plaques on the neuronal surfaces in
the brain.4 Others feel the disease is a result of the entanglement of neurons caused by the degeneration and destruction
of Tau proteins.5 However, both groups can agree that both
beta amyloid and Tau protein play a key role in AD development and progression.

Beta Amyloid Plaques
Beta Secretase (BACE) inhibitors (Table 1) are drugs that
have been in development over the past few years. These
drugs target the enzyme Beta-secretase, which is responsible
for one of the 2 important cleavage steps in the formation of
amyloid-β peptides.6 The accumulation of these amyloid-β
peptides is what researchers have theorized to be one of the
essential causes for the development of AD.5 Unfortunately,
recent Phase III studies, such as a late-phase verubecestat
study, have not shown a benefit to patients with established
mild-to-moderate AD. Results such as these are forcing drug
companies to look into new target areas for the disease.
However, a few BACE inhibitors still have ongoing trials in
early AD. Researchers are hoping that by catching the
buildup of beta amyloid early, they will stop the progression
1

St. Louis College of Pharmacy, MO, USA
Prescribe Right, LLC, Wildwood, MO, USA

2

New Treatment Options
A definitive pathophysiology on the development of AD has
not been determined. One theory is that AD is due to the

Corresponding Author:
Scot Walker, Chief Executive Officer, Prescribe Right, LLC,
1602 Westglen Farms Dr, Wildwood, MO 63011, USA.
Email: scot.walker@prescriberight.com
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