Increased Prevalence of Obesity/Type 2 Diabetes and Lower Levels of Lithium in Rural Texas Counties May Explain Greater Alzheimer’s Disease Risk

Baranowski, Bradley J.; Hayward, Grant C.; Fajardo, Val Andrei; MacPherson, Rebecca E. K.

doi:10.3233/jad-171150

Cited by 14 publications

(12 citation statements)

References 27 publications

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“…Indeed, external risk factors including smoking, hypertension, depression, insulin resistance, diabetes, and obesity have been shown to account for ≈50% of all reported cases when combined [ 1 ]. Even improper sleep has been linked to increased risk of AD [ 9 , 10 ]. Many of these risk factors, such as T2D and obesity, contribute to what is described as metabolic dysregulation [ 11 , 12 ].…”

Section: Alzheimer’s Diseasementioning

confidence: 99%

Resveratrol, Metabolic Dysregulation, and Alzheimer’s Disease: Considerations for Neurogenerative Disease

Yang

Bagit

MacPherson

2021

IJMS

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Alzheimer’s disease (AD) has traditionally been discussed as a disease where serious cognitive decline is a result of Aβ-plaque accumulation, tau tangle formation, and neurodegeneration. Recently, it has been shown that metabolic dysregulation observed with insulin resistance and type-2 diabetes actively contributes to the progression of AD. One of the pathologies linking metabolic disease to AD is the release of inflammatory cytokines that contribute to the development of brain neuroinflammation and mitochondrial dysfunction, ultimately resulting in amyloid-beta peptide production and accumulation. Improving these metabolic impairments has been shown to be effective at reducing AD progression and improving cognitive function. The polyphenol resveratrol (RSV) improves peripheral metabolic disorders and may provide similar benefits centrally in the brain. RSV reduces inflammatory cytokine release, improves mitochondrial energetic function, and improves Aβ-peptide clearance by activating SIRT1 and AMPK. RSV has also been linked to improved cognitive function; however, the mechanisms of action are less defined. However, there is evidence to suggest that chronic RSV-driven AMPK activation may be detrimental to synaptic function and growth, which would directly impact cognition. This review will discuss the benefits and adverse effects of RSV on the brain, highlighting the major signaling pathways and some of the gaps surrounding the use of RSV as a treatment for AD.

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Section: Alzheimer’s Diseasementioning

confidence: 99%

Resveratrol, Metabolic Dysregulation, and Alzheimer’s Disease: Considerations for Neurogenerative Disease

Yang

Bagit

MacPherson

2021

IJMS

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“…Fatty acids are categorized into saturated fatty acids (SFA) and unsaturated fatty acids, which can be further grouped into mono-(MUFA) and polyunsaturated (PUFA) fatty acids. High intake of SFA is not only related to an increased risk of metabolic disorders like type 2 diabetes mellitus (T2DM), but also AD (Baranowski et al 2018b;de la Monte and Wands 2008;Profenno et al 2010). For example, cross-sectional (Kalmijn et al 2004) and longitudinal population-based studies have found positive correlations between increased SFA intake and a higher risk of mild cognitive impairment (MCI) and AD (Kalmijn et al 1997;Morris et al 2003).…”

Section: Western Dietmentioning

confidence: 99%

“…Regular exercise is another lifestyle factor that not only combats obesity and related metabolic diseases but also reduces the risk of AD (de Bruijn et al 2013;Ogino et al 2019). Epidemiological studies highlight positive correlations between physical inactivity and AD mortality rates (Baranowski et al 2018b;Laurin et al 2001). In agreement with these findings, a systematic review examining the role of physical activity as a potential preventative intervention for AD confirmed that there is an inverse association between physical activity and the risk of AD.…”

Section: Exercise and Admentioning

confidence: 99%

Healthy brain, healthy life: a review of diet and exercise interventions to promote brain health and reduce Alzheimer’s disease risk

Baranowski

Markó

Fenech

et al. 2020

Appl. Physiol. Nutr. Metab.

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With the world’s population aging at a rapid rate, the prevalence of Alzheimer’s disease (AD) has significantly increased. These statistics are alarming given recent evidence that a third of dementia cases may be preventable. The role of lifestyle factors, such as diet and exercise, can directly alter the risk of disease development. However, an understanding of the effectiveness of dietary patterns and exercise strategies to reduce AD risk or improve brain function is not fully understood. The aim of this review is to discuss the effects of diet and exercise on AD risk. Key components of the Western and Mediterranean diets are discussed in relation to AD progression, as well as how physical activity promotes brain health. Components of the Western diet (saturated fatty acids and simple carbohydrates) are detrimental to the brain, impair cognition and increase AD pathologies. While components of the Mediterranean diet, (polyunsaturated fatty acids, polyphenols, and antioxidants) are considered to be neuroprotective. Exercise can significantly reduce the risk of AD, however specific exercise recommendations for older adults are limited and optimal intensity, duration, and type remains unknown. This review highlights important modifiable risk factors for AD and points out potential avenues for future research. Novelty Bullets •Diet and exercise are modifiable factors that can improve brain health and reduce the risk of Alzheimer’s disease •Polyunsaturated fatty acids, polyphenols, and antioxidants are considered to be neuroprotective •Exercise reduces neuroinflammation, improves brain insulin sensitivity, and increases BDNF

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“…Clinical and epidemiological evidence highlights the fact that lifestyle factors, such as diet and exercise, are crucial in reducing the risk of late onset Alzheimer’s disease ( de la Monte and Wands, 2008 ; Pasinetti and Eberstein, 2008 ; Vagelatos and Eslick, 2013 ; Baranowski et al, 2018b , 2020 ). The accumulation of amyloid beta (Aβ) plaques is a pathological hallmark of Alzheimer’s disease ( Behl and Holsboer, 1998 ).…”

Section: Introductionmentioning

confidence: 99%

“…Epidemiological studies have identified physical inactivity and obesity as significant risk factors for Alzheimer’s disease mortality rates and disease progression ( Profenno et al, 2010 ; Baranowski et al, 2018b ). In humans, there appears to be a relationship between obesity and circulating plasma Aβ ( Mayeux et al, 2003 ; Balakrishnan et al, 2005 ; Luciano et al, 2015 ), along with evidence to support that higher levels of plasma Aβ can be used to predict the risk of developing Alzheimer’s disease and cognitive impairments ( Ida et al, 1996 ; Mayeux et al, 2003 ; Mayeux and Schupf, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

Examination of BDNF Treatment on BACE1 Activity and Acute Exercise on Brain BDNF Signaling

Baranowski

Hayward

Markó

et al. 2021

Front. Cell. Neurosci.

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Perturbations in metabolism results in the accumulation of beta-amyloid peptides, which is a pathological feature of Alzheimer’s disease. Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is the rate limiting enzyme responsible for beta-amyloid production. Obesogenic diets increase BACE1 while exercise reduces BACE1 activity, although the mechanisms are unknown. Brain-derived neurotropic factor (BDNF) is an exercise inducible neurotrophic factor, however, it is unknown if BDNF is related to the effects of exercise on BACE1. The purpose of this study was to determine the direct effect of BDNF on BACE1 activity and to examine neuronal pathways induced by exercise. C57BL/6J male mice were assigned to either a low (n = 36) or high fat diet (n = 36) for 10 weeks. To determine the direct effect of BDNF on BACE1, a subset of mice (low fat diet = 12 and high fat diet n = 12) were used for an explant experiment where the brain tissue was directly treated with BDNF (100 ng/ml) for 30 min. To examine neuronal pathways activated with exercise, mice remained sedentary (n = 12) or underwent an acute bout of treadmill running at 15 m/min with a 5% incline for 120 min (n = 12). The prefrontal cortex and hippocampus were collected 2-h post-exercise. Direct treatment with BDNF resulted in reductions in BACE1 activity in the prefrontal cortex (p < 0.05), but not the hippocampus. The high fat diet reduced BDNF content in the hippocampus; however, the acute bout of exercise increased BDNF in the prefrontal cortex (p < 0.05). These novel findings demonstrate the region specific differences in exercise induced BDNF in lean and obese mice and show that BDNF can reduce BACE1 activity, independent of other exercise-induced alterations. This work demonstrates a previously unknown link between BDNF and BACE1 regulation.

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Increased Prevalence of Obesity/Type 2 Diabetes and Lower Levels of Lithium in Rural Texas Counties May Explain Greater Alzheimer’s Disease Risk

Abstract: AD mortality rates are higher in rural counties when compared to urban counties, and this may be linked to greater physical inactivity, obesity, and diabetes, as well as lower trace lithium levels in tap water.

Cited by 14 publications

References 27 publications

Resveratrol, Metabolic Dysregulation, and Alzheimer’s Disease: Considerations for Neurogenerative Disease

Resveratrol, Metabolic Dysregulation, and Alzheimer’s Disease: Considerations for Neurogenerative Disease

Healthy brain, healthy life: a review of diet and exercise interventions to promote brain health and reduce Alzheimer’s disease risk

Examination of BDNF Treatment on BACE1 Activity and Acute Exercise on Brain BDNF Signaling

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