Now you need your doctors and hospital to initiate human research in this and specify how these newly created neurons will migrate to needed areas.
Maybe these might help:
Intermittent fasting increases adult hippocampal neurogenesis
Associated Data
Abstract
Introduction
Intermittent
fasting (IF) has been suggested to have neuroprotective effects through
the activation of multiple signaling pathways. Rodents fasted
intermittently exhibit enhanced hippocampal neurogenesis and long‐term
potentiation (LTP) at hippocampal synapses compared with sedentary
animals fed an ad libitum (AL) diet. However, the underlying mechanisms
have not been studied. In this study, we evaluated the mechanistic gap
in understanding IF‐induced neurogenesis.
Methods
We
evaluated the impact of 3 months of IF (12, 16, and 24 hr of food
deprivation on a daily basis) on hippocampal neurogenesis in C57BL/6NTac
mice using immunoblot analysis.
Results
Three‐month
IF significantly increased activation of the Notch signaling pathway
(Notch 1, NICD1, and HES5), neurotrophic factor BDNF, and downstream
cellular transcription factor, cAMP response element‐binding protein
(p‐CREB). The expression of postsynaptic marker, PSD95, and neuronal
stem cell marker, Nestin, was also increased in the hippocampus in
response to 3‐month IF.
Conclusions
These findings suggest that IF may increase hippocampal neurogenesis involving the Notch 1 pathway.
Keywords: brain‐derived neurotrophic factor, hippocampus, intermittent fasting, neurogenesis, Notch
Abstract
Intermittent
fasting (IF) is a dietary protocol where energy restriction is induced
by alternate periods of ad libitum feeding and fasting. The present
study has sought to investigate the relationship between IF and
hippocampal neurogenesis. Our findings suggest that IF may increase
hippocampal neurogenesis involving the Notch 1 pathway.
1. INTRODUCTION
Dietary
restriction (DR) is defined as a decrease in energy consumption without
reducing nutritional value. This simple dietary intervention has been
shown in a wide range of experimental animals to extend lifespan and
decrease the incidence of several age‐related diseases. The definition
of DR has been expanded from an alternative description of caloric
restriction (CR) to also encompass a broader scope of interventions,
including short‐term starvation, periodic fasting, fasting‐mimetic
diets, and intermittent fasting (IF; Mattson & Arumugam, 2018).
IF has been proven to be advantageous to various organ systems in the
body and acts as a mild metabolic stressor. It has been postulated that
IF is able to cause powerful changes in the metabolic pathways in the
brain via an increase in stress resistance, and breakdown of ketogenic
amino acids and fatty acids (Bruce‐Keller, Umberger, McFall, &
Mattson, 1999; Kim et al., 2018).
Experimental studies have also shown that IF is neuroprotective against
acute brain injuries such as stroke, and neurodegenerative diseases
(Arumugam et al., 2010; Halagappa et al., 2007; Manzanero et al., 2014).
In addition, recent studies have also shown that IF can lead to an
increase in neurogenesis levels in the hippocampus (Manzanero et al., 2014).
In
the adult brain, the niches of neuronal stem cells (NSCs) are located
specifically at the subventricular zone (SVZ) of the lateral ventricles,
and in the subgranular zone (SGZ) of the hippocampus. The ability of
NSCs to maintain cerebral neurogenesis is controlled by the tight
regulation of balanced events commencing from stem cell maintenance, to
stem cell division and proliferation, to its differentiation into mature
neurons, and finally their survival and functional integration into the
brain parenchyma (Lathia, Mattson, & Cheng, 2008; Lledo, Alonso, & Grubb, 2006).
The process of adult neurogenesis is highly regulated and is adaptable
to environmental, morphological, and physiological cues, whereby
cerebral performance is suited to function at optimal levels for a given
environment. Studies have demonstrated that the proliferation of neural
stem cells can be modified through metabolic perturbations experienced
during high temperatures (Matsuzaki et al., 2009), physical activity (Niwa et al., 2016), and a high‐fat diet (Kokoeva, Yin, & Flier, 2005).
Experimental studies from our group have also shown that IF increases
neurogenesis in the hippocampus as a form of neuroprotection following
acute brain injury such as ischemic stroke. Moreover, we established
that the number of BrdU‐labeled cells in the dentate gyrus of IF mice
was elevated (Manzanero et al., 2014).
To measure cell proliferation without the confound availability of an
exogenous marker BrdU, we established increases in the number of
Ki67‐labeled cells in the dentate gyrus of mice on the IF diet,
indicating enhancement of cell proliferation in these mice (Manzanero et
al., 2014).
In addition to our findings, previous work similarly demonstrated that
using the every other day (EOD) IF regimen also increased BrdU‐labeled
cell number in the hippocampus (Lee, Duan, & Mattson, 2002).
However,
the molecular process involved in IF‐induced neurogenesis is not well
understood. The Notch signaling pathway that is intricately involved in
the determination of cell fate during brain development and adult
neurogenesis may be a possible molecular process involved in IF‐induced
neurogenesis (Lathia et al., 2008).
In this study, we investigated the expression levels of molecular and
cellular components of the hippocampal region, focusing specifically on
Notch activation and associated proteins that are known to promote
hippocampal neurogenesis such as brain‐derived neurotrophic factor
(BDNF) and cAMP response element‐binding protein (CREB).
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