I'm doing a 325 aspirin for blood thinning. WHOM DO I ASK IF THIS IS THE RIGHT AMOUNT TO GENERATE HUMAN NEUROGENESIS?
A Mild Dose of Aspirin Promotes Hippocampal Neurogenesis and Working Memory in Experimental Ageing Mice
1,3,*
1
Laboratory of Stem Cells and
Neuroregeneration, Department of Animal Science, School of Life
Sciences, Bharathidasan University, Tiruchirappalli 620024, India
2
Molecular Neuro-Gerontology Laboratory,
Department of Biochemistry, School of Life Sciences, Bharathidasan
University, Tiruchirappalli 620024, India
3
University Grants Commission-Faculty Recharge Programme (UGC-FRP), New Delhi 110002, India
*
Author to whom correspondence should be addressed.
Brain Sci. 2023, 13(7), 1108; https://doi.org/10.3390/brainsci13071108
Received: 14 June 2023
/
Revised: 16 July 2023
/
Accepted: 17 July 2023
/
Published: 21 July 2023
(This article belongs to the Special Issue Neuroregenerative Plasticity in Health and Disease)
Abstract
Aspirin has been reported to prevent memory decline
in the elderly population. Adult neurogenesis in the hippocampus has
been recognized as an underlying basis of learning and memory. This
study investigated the effect of aspirin on spatial memory in
correlation with the regulation of hippocampal neurogenesis and
microglia in the brains of ageing experimental mice. Results from the
novel object recognition (NOR) test, Morris water maze (MWM), and cued
radial arm maze (cued RAM) revealed that aspirin treatment enhances
working memory in experimental mice. Further, the co-immunohistochemical
assessments on the brain sections indicated an increased number of
doublecortin (DCX)-positive immature neurons and bromodeoxyuridine
(BrdU)/neuronal nuclei (NeuN) double-positive newly generated neurons in
the hippocampi of mice in the aspirin-treated group compared to the
control group. Moreover, a reduced number of ionized calcium-binding
adaptor molecule (Iba)-1-positive microglial cells was evident in the
hippocampus of aspirin-treated animals. Recently, enhanced activity of
acetylcholinesterase (AChE) in circulation has been identified as an
indicative biomarker of dementia. The biochemical assessment in the
blood of aspirin-treated mice showed decreased activity of AChE in
comparison with that of the control group. Results from this study
revealed that aspirin facilitates hippocampal neurogenesis which might
be linked to enhanced working memory.
1. Introduction
Aspirin
is one of the most widely used generic non-steroidal anti-inflammatory
drugs (NSAIDs) in the treatment regime of pain and fever [1,2].
Regular intake of aspirin provides preventive measures against various
ageing-associated diseases including cardiovascular illness, cerebral
stroke, thrombosis, and cancer [3].
The blockade of the cyclooxygenase (COX)-2 enzyme responsible for the
synthesis of inflammatory prostaglandins is a well-recognized mode of
action for aspirin [4].
While various mood disorders, neurocognitive deficits, and psychiatric
illnesses have been characterized by overexpression of COX-2 in
association with, neuroinflammation and oxidative stress in the brain,
pharmacological blockade of COX-2 has been considered a crucial
neurotherapeutic intervention [5,6].
Among various COX-2 inhibitors, aspirin treatment has been speculated
to enhance memory in the ageing population and mitigate
neuropathogenesis in subjects with various brain diseases. While some
correlative studies indicated that the association between aspirin
treatment and memory is uncertain, ample scientific evidence strongly
implies that aspirin prevents memory decline in elderly subjects [7,8].
Eventually, recent reports demonstrated that aspirin treatment
considerably improves the synaptic plasticity in the cognitive centers
of the experimental brains [9].
Moreover, the implementation of aspirin has been considered for the
treatment regime of memory loss in ageing and neurodegenerative
disorders including Alzheimer’s disease (AD) [10,11].
However, the underlying cellular mechanism through which aspirin
modulates neuroplasticity responsible for neurocognitive measures
remains unclear. Adult neurogenesis is an inimitable neuroregenerative
process in which new functional neurons are continuously generated from
neural stem cells (NSCs) in the hippocampus and subventricular zone
(SVZ)olfactory bulb (OB) system of the brain [12,13,14].
Notably, the occurrence of neurogenesis in the hippocampus has been
identified to provide the cellular basis of pattern separation, mood,
spatial learning, and working memory in physiological conditions [15,16]. In contrast, memory loss upon ageing has been attributed to decreased hippocampal neurogenesis [17].
Moreover, neurodegenerative disorders have been characterized by
impaired hippocampal neurogenesis due to chronic neuroinflammation
accounting for various neurological deficits and dementia [12,13,18].
Therefore, targeting a centralized neuroinflammatory pathway such as
COX signaling that interlinks different pathogenic mechanisms and
suppresses the hippocampal neuroregenerative plasticity during ageing
and neuropathogenic conditions has become an unmet therapeutic need for
progressive memory loss. Considering its prominent COX inhibitory
potential aspirin treatment can be presumed to be involved in the
regulation of hippocampal neurogenesis in the brain that could
facilitate a positive impact in boosting learning and memory. However,
the scientific evidence for the effects of aspirin on the regulation of
neuroregenerative potential of the brain associated with memory
functions is highly limited. While aspirin has been consumed by a
considerable number of individuals worldwide, understanding the
neuropharmacological effects of aspirin on the modulation of
neuroplasticity and neuroregenerative measures accountable for memory
functions is an important scientific perusal at the preclinical state.
Therefore, this study investigated the effect of aspirin on the
regulation of hippocampal neurogenesis and neurocognitive behaviors in
experimental ageing mice.
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