Page 68 - Petelin, Ana, Nejc Šarabon, Boštjan Žvanut, eds. 2017. Zdravje delovno aktivne populacije ▪︎ Health of the Working-Age Population. Proceedings. Koper: Založba Univerze na Primorskem/University of Primorska Press
P. 68
avje delovno aktivne populacije | health of the working-age population 66 er before pathologies and symptoms appear – and is much greater than in nor-
mal aging (Costantini et al., 2008). The changed metabolic environment rein-
forces the disease progression. Normalization of bioenergetics can be efficient
in treatment neurological diseases (Masino et al., 2008, Zilberter et al., 2017).
AD is the most common type of dementia; it features accumulation of
amyloid plaques and hyperphosphorylation of tau protein resulting in inflam-
matory response and oxidative stress. The mechanism is not well understood,
but it seems that type 2 diabetes (T2D) accelerates these processes. Cerebral at-
rophy, hypometabolism of glucose and insulin resistance are featured in both
diseases (Verdile et al., 2015). Cognitive decline is directly correlated to the level
of glucose hypometabolism (de Leon et al., 1983). Some authors claim that AD
is a type 3 diabetes (de la Monte et al., 2008).
In animal models of AD, nutritional ketosis can ameliorate the extent of
beta amyloid plaque accumulation (Krikorian et al., 2012). However, with pa-
tients without ApoE4 allele one of the nutritional options to improve mild cog-
nitive impairments is adding medium chain triglycerides to the diet (Page et
al., 2009, Farias et al., 2014, Sharma et al., 2014, Fernando et al., 2015, Hertz et
al., 2015, Ohnuma et al., 2016).
Even in the excessive ROS model of AD, the KD is still useful as an an-
tioxidative therapy. There is mixed evidence about the oxidative stress as the
ground for AD in clinical trials, but it is possible that the antioxidant thera-
pies did not succeed to deliver the antioxidants where they should be delivered
(Rosini et al., 2014). KD might have been more successful.
KB help decrease the oxidative stress, while also being a substrate for en-
ergy. Both roles make KB highly neuroprotective agents (Cahill, 2006). KB me-
diate their antioxidative properties by activation of protective transcription
factors (like Nrf2) that increase the production of antioxidants like glutathione
and other enzymes (Milder et al., 2012).
In KD, the metabolism of astrocytes producing purines (ATP and adenos-
ine) is increased (Masino et al., 2008, Boison, 2013). In animal models there is
increased autophagy of neurons in ketotic environment (McCarty et al., 2015).
Balancing excitotoxicity and cell death as a consequence can have a bene-
ficial effect with patients who survived ischemic stroke and death of mitochon-
dria that takes place sometime later after the event. In animal models these
devastation to mitochondria can be alleviated by KB (Baxter et al., 2014). Post-
operatively, KD could also be used with adult patients who suffered head trau-
ma (Prins et al., 2014).
Discussion
Effects of KD are profound, but also complex. Yet applying any therapeutic
means to affect the nervous system is rarely straightforward and simple to ob-
serve.
mal aging (Costantini et al., 2008). The changed metabolic environment rein-
forces the disease progression. Normalization of bioenergetics can be efficient
in treatment neurological diseases (Masino et al., 2008, Zilberter et al., 2017).
AD is the most common type of dementia; it features accumulation of
amyloid plaques and hyperphosphorylation of tau protein resulting in inflam-
matory response and oxidative stress. The mechanism is not well understood,
but it seems that type 2 diabetes (T2D) accelerates these processes. Cerebral at-
rophy, hypometabolism of glucose and insulin resistance are featured in both
diseases (Verdile et al., 2015). Cognitive decline is directly correlated to the level
of glucose hypometabolism (de Leon et al., 1983). Some authors claim that AD
is a type 3 diabetes (de la Monte et al., 2008).
In animal models of AD, nutritional ketosis can ameliorate the extent of
beta amyloid plaque accumulation (Krikorian et al., 2012). However, with pa-
tients without ApoE4 allele one of the nutritional options to improve mild cog-
nitive impairments is adding medium chain triglycerides to the diet (Page et
al., 2009, Farias et al., 2014, Sharma et al., 2014, Fernando et al., 2015, Hertz et
al., 2015, Ohnuma et al., 2016).
Even in the excessive ROS model of AD, the KD is still useful as an an-
tioxidative therapy. There is mixed evidence about the oxidative stress as the
ground for AD in clinical trials, but it is possible that the antioxidant thera-
pies did not succeed to deliver the antioxidants where they should be delivered
(Rosini et al., 2014). KD might have been more successful.
KB help decrease the oxidative stress, while also being a substrate for en-
ergy. Both roles make KB highly neuroprotective agents (Cahill, 2006). KB me-
diate their antioxidative properties by activation of protective transcription
factors (like Nrf2) that increase the production of antioxidants like glutathione
and other enzymes (Milder et al., 2012).
In KD, the metabolism of astrocytes producing purines (ATP and adenos-
ine) is increased (Masino et al., 2008, Boison, 2013). In animal models there is
increased autophagy of neurons in ketotic environment (McCarty et al., 2015).
Balancing excitotoxicity and cell death as a consequence can have a bene-
ficial effect with patients who survived ischemic stroke and death of mitochon-
dria that takes place sometime later after the event. In animal models these
devastation to mitochondria can be alleviated by KB (Baxter et al., 2014). Post-
operatively, KD could also be used with adult patients who suffered head trau-
ma (Prins et al., 2014).
Discussion
Effects of KD are profound, but also complex. Yet applying any therapeutic
means to affect the nervous system is rarely straightforward and simple to ob-
serve.
