Authors :
Anya Gurudatt; Alicia Van Enoo
Volume/Issue :
Volume 8 - 2023, Issue 8 - August
Google Scholar :
https://bit.ly/3TmGbDi
Scribd :
https://tinyurl.com/4fzue62p
DOI :
https://doi.org/10.5281/zenodo.8363069
Abstract :
This paper will be a review of current and
ongoing literature surrounding how the aggregation of
amyloid-β can induce cognitive impairment, neuronal loss,
and the overall pathogenesis of Alzheimer’s disease
through its interactions with glutamate receptors,
microglia, tau proteins, and lipid rafts. Through these
mechanisms of action, amyloid-β can induce synaptic
dysfunction, neuroinflammation, neurotoxicity, impaired
synaptic plasticity, and other issues that worsen AD-
associated neurodegeneration. Multiple preclinical studies
have been conducted to better understand these
mechanisms as potential targets for therapeutic
intervention. Unfortunately, when tested in clinical trials,
drugs targeting amyloid-β have consistently failed.
However, there are still futures for various ongoing clinical
trials targeted at dissolving soluble and insoluble amyloid-
β deposits, reducing the production of amyloid-β, and
preventing amyloid-β aggregation, specifically: passive
vaccination, monoclonal antibodies, and γ-secretase
inhibitors. Monoclonal antibodies, in particular, have
proven to be most promising. This paper reviews some of
the most novel and recent findings and their implications
for the future of the field. This paper will also evaluate the
most promising forms of therapeutic intervention that
have been and are currently being investigated, as well as
limitations and future prospects of targeting amyloid-β to
slow the progression of Alzheimer’s disease.
This paper will be a review of current and
ongoing literature surrounding how the aggregation of
amyloid-β can induce cognitive impairment, neuronal loss,
and the overall pathogenesis of Alzheimer’s disease
through its interactions with glutamate receptors,
microglia, tau proteins, and lipid rafts. Through these
mechanisms of action, amyloid-β can induce synaptic
dysfunction, neuroinflammation, neurotoxicity, impaired
synaptic plasticity, and other issues that worsen AD-
associated neurodegeneration. Multiple preclinical studies
have been conducted to better understand these
mechanisms as potential targets for therapeutic
intervention. Unfortunately, when tested in clinical trials,
drugs targeting amyloid-β have consistently failed.
However, there are still futures for various ongoing clinical
trials targeted at dissolving soluble and insoluble amyloid-
β deposits, reducing the production of amyloid-β, and
preventing amyloid-β aggregation, specifically: passive
vaccination, monoclonal antibodies, and γ-secretase
inhibitors. Monoclonal antibodies, in particular, have
proven to be most promising. This paper reviews some of
the most novel and recent findings and their implications
for the future of the field. This paper will also evaluate the
most promising forms of therapeutic intervention that
have been and are currently being investigated, as well as
limitations and future prospects of targeting amyloid-β to
slow the progression of Alzheimer’s disease.
