Decline in Weight and Incident Mild Cognitive Impairment

Alhurani, Rabe E.; Vassilaki, Maria; Aakre, Jeremiah A.; Mielke, Michelle M.; Kremers, Walter K.; Machulda, Mary M.; Geda, Yonas E.; Knopman, David S.; Peterson, Ronald C.; Roberts, Rosebud O.

doi:10.1001/jamaneurol.2015.4756

Cited by 102 publications

(86 citation statements)

References 48 publications

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“…education background, handgrip strength, GDS and albumin) were significantly associated with MCI, indicating the validity of the participant population and data in the present study. [16][17][18] In terms of age, the present findings contradict the results of previous studies, as we observed a significantly lower incidence of MCI with increasing age. 18,19 In fact, although some reports have found no significant association between age and MCI, no study has shown a lower incidence of cognitive impairment with increasing age.…”

Section: Discussioncontrasting

confidence: 99%

“…Consistent with previous studies, we found that various factors (e.g. education background, handgrip strength, GDS and albumin) were significantly associated with MCI, indicating the validity of the participant population and data in the present study . In terms of age, the present findings contradict the results of previous studies, as we observed a significantly lower incidence of MCI with increasing age .…”

Section: Discussionsupporting

confidence: 87%

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Oral function as an indexing parameter for mild cognitive impairment in older adults

Watanabe

Arai

Hirano

et al. 2018

Geriatrics Gerontology Int

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 87%

Oral function as an indexing parameter for mild cognitive impairment in older adults

Watanabe

Arai

Hirano

et al. 2018

Geriatrics Gerontology Int

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“…Though there is some controversy (one study reported that lower weight in later life predicts MCI 19 and another demonstrated no increase of MCI risk with high BMI 20 ) the majority of studies indicate that a high BMI is associated with attention deficits, poor executive function, impaired decision-making, and decreased verbal learning and memory. Individuals with severe obesity have MCI, 21 and obese children and adolescents, as well as those with MetS, 22 display lower cognitive function, 23 further distinguishing obesity-associated MCI from age-related dementia.…”

Section: Effects Of Obesity On the Central Nervous Systemmentioning

confidence: 99%

Neurological consequences of obesity

O’Brien

Hinder

Callaghan

et al. 2017

The Lancet Neurology

378

261

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Obesity, primarily a consequence of poor dietary choices and an increased sedentary lifestyle, has become a global pandemic that brings with it enormous medical, social, and economic challenges. Not only does obesity increase the risk of cardiovascular disease and certain cancers, but it is also recognized as a key driver of other metabolic syndrome (MetS) components. These components include insulin resistance, hyperglycemia with prediabetes or type 2 diabetes, dyslipidemia, and hypertension, and are underlying contributors to systemic metabolic dysfunction. More recently, obesity and diet-induced metabolic dysfunction have been identified as risk factors for the development of a wide variety of neurological disorders in both the central and peripheral nervous systems. An abundance of literature has shown that obesity is associated with mild cognitive impairment and altered hippocampal structure and function, and there is a robust correlation between obesity and Alzheimer’s type dementia. Similarly, many reports show that both the autonomic and somatic components of the peripheral nervous system are impacted by obesity. The autonomic nervous system, under control of the hypothalamus, displays altered catabolic and anabolic processes in obese individuals attributed to sympathetic-parasympathetic imbalances. A close association also exists between obesity and polyneuropathy, a complication most commonly found in prediabetic and diabetic patients, and is likely secondary to a combination of obesity-induced dyslipidemia with hyperglycemia. This review will outline the pathophysiological development of obesity and dyslipidemia, discuss the adverse impact of these conditions on the nervous system, and provide evidence for lipotoxicity and metabolic inflammation as the drivers underlying the neurological consequences of obesity. In addition, this review will examine the benefits of lifestyle and surgical interventions in obesity-induced neurological disorders.

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“…Loss of body weight can occur as mice reach old age (Alhurani et al, ; Goodrick, Ingram, Reynolds, Freeman, & Cider, ; Samorajski et al, ). Hat1 +/− mice displayed a reduced size at birth that became less pronounced by 5 weeks of age (Nagarajan et al, ).…”

Section: Resultsmentioning

confidence: 99%

Early‐onset aging and mitochondrial defects associated with loss of histone acetyltransferase 1 (Hat1)

et al. 2019

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Histone acetyltransferase 1 (Hat1) is responsible for the acetylation of newly synthesized histone H4 on lysines 5 and 12 during the process of chromatin assembly. To understand the broader biological role of Hat1, we have generated a conditional mouse knockout model of this enzyme. We previously reported that Hat1 is required for viability and important for mammalian development and genome stability. In this study, we show that haploinsufficiency of Hat1 results in a significant decrease in lifespan. Defects observed in Hat1+/− mice are consistent with an early‐onset aging phenotype. These include lordokyphosis (hunchback), muscle atrophy, minor growth retardation, reduced subcutaneous fat, cancer, and paralysis. In addition, the expression of Hat1 is linked to the normal aging process as Hat1 mRNA and protein becomes undetectable in many tissues in old mice. At the cellular level, fibroblasts from Hat1 haploinsufficient embryos undergo early senescence and accumulate high levels of p21. Hat1+/− mouse embryonic fibroblasts (MEFs) display modest increases in endogenous DNA damage but have significantly higher levels of reactive oxygen species (ROS). Consistently, further studies show that Hat1−/− MEFs exhibit mitochondrial defects suggesting a critical role for Hat1 in mitochondrial function. Taken together, these data show that loss of Hat1 induces multiple hallmarks of early‐onset aging.

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Decline in Weight and Incident Mild Cognitive Impairment

Cited by 102 publications

References 48 publications

Oral function as an indexing parameter for mild cognitive impairment in older adults

Oral function as an indexing parameter for mild cognitive impairment in older adults

Neurological consequences of obesity

Early‐onset aging and mitochondrial defects associated with loss of histone acetyltransferase 1 (Hat1)

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