Brain-derived neurotrophic factor (
BDNF), or
abrineurin, is a member of the
neurotrophin family of
growth factors that acts on both the central and peripheral nervous systems.
BDNF is also well known for its cardinal role in normal neural maturation. It binds to at least two receptors at the cell surface known as
tyrosine kinase B (TrkB) and p75NTR. Additional
neurotrophins that are anatomically linked with
BDNF include neurotrophin-3 (NT-3),
neurotrophin-4 (NT-4), and
nerve growth factor (
NGF). It is evident that
BDNF levels in patients with
Alzheimer's disease (AD) are altered. AD is a progressive disorder and a form of
dementia, where the mental function of an elderly person is disrupted. It is associated with a progressive decline in cognitive function, which mainly targets the thinking, memory, and behavior of the person. The degeneration of neurons occurs in the cerebral cortex region of brain. The two major sources responsible for neuronal degeneration are
protein fragment
amyloid-beta (Aβ), which builds up in the spaces between the nerve cells, known as plaques, disrupting the neuron signaling pathway and leading to
dementia, and neurofibrillary tangles (NFTs), which are the twisted fibers of
proteins that build up inside the cells. AD is highly prevalent, with recent data indicating nearly 5.8 million Americans aged 65 and older with AD in 2020, and with 80% of patients 75 and older. AD is recognized as the sixth leading cause of death in the USA, and its prevalence is predicted to increase exponentially in the coming years. As AD worsens over time, it becomes increasingly important to understand the exact pathophysiology,
biomarkers, and treatment. In this article, we focus primarily on the controversial aspect of
BDNF in AD, including its influence on various other
proteins and
enzymes and the current treatments associated with
BDNF, along with future perspectives.