Alzheimer’s disease (AD) is a chronic multifactorial and
complex neuro-degenerative disorder characterized by memory impairment and loss
of cognitive ability which is a plight for the elderly. AD is an aging brain
pathology, and maybe it is a combination of different diseases or various
symptoms that are orchestrated in common. Alzheimer’s disease is the most
common type of dementia and it may contribute to 60–70% of cases.
Pathologically intracellular accumulation of abnormally phosphorylated Tau
protein to form neurofibrillary tangles, extracellular amyloid-beta (Aβ) deposition
to form senile plaques, neural disconnection, neural deaths and synaptic
dysfunction within the brain are hallmark pathologies that characterize AD. The
prevalence of the disease continues to increase globally due to the increase in
longevity, quality of life, and medical treatment for chronic diseases that
decrease mortality and enhance the survival among elderly. Medical awareness
and accurate diagnosis of the disease also contribute to the high prevalence
observed globally. Unfortunately, no magic treatment exists to modify the
course of AD, and no available treatment is capable to mitigate the cognitive
decline or reversing the pathology of the disease yet.
A Plethora of hypothesis beginning from cholinergic to the
dominant Aβ cascade hypothesis to the abnormally excessive phosphorylated Tau
protein were reported. Various explanations for the pathogenesis of AD such as
abnormal excitation of glutamate system and mitochondrial dysfunction were also
suggested. Despite the continuous stumble to deliver significant benefits and
effective treatment for this agonizing global aging illness, multiprong
approaches and strategies to ameliorate the disease course are urgently needed
based on the knowledge of the underpinning pathogenesis of AD.
Immunosenescence is a procedure of immune deficit that
appears with age (inflammaging process) and encompasses remodeling of lymphoid
organs, leading to alterations in the immune function and neuroinflammation in
advanced aging, which is closely linked to the outgrowth of infections,
autoimmune diseases, and malignant cancers. It is well known that long-standing
inflammation influence badly the brain over the course of a lifetime due to the
senescence of the immune system.
Herein, we want to trace the role of the immune system in
the pathogenesis of AD, thus we are going to explore alternative avenues, such
as neuroimmune involvement in the pathogenesis of AD. Determination of the
initial triggers engaged in neuroinflammation, which is an early episode of the
presymptomatic stages of AD and contributes to the advancement of the disease
and the underlying key mechanisms of brain damage that might help the
development of therapeutic strategies to combat this devastating disease. In
addition, this study represents how different aspects of the immune system,
both in the brain and peripherally, behave to contribute to AD.
Author(s) Details:
Abdalla Bowirrat,
Department of Molecular Biology, Adelson School of Medicine, Ariel
University, Ariel 40700, Israel.
Aia Bowirrat M. D.,
Department
of Orthopedic Surgery, Hasharon Hospital, Rabin Medical Center, Petah Tikwa,
Israel.
Please see the link here: https://stm.bookpi.org/NVMMS-V5/article/view/14150
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