Brain-Derived Neurotrophic Factor Plasma Levels: Relationship With Dementia and Diabetes in the Elderly Population

Passaro, Angelina; Nora, Edoardo Dalla; Morieri, Mario Luca; Soavi, Cecilia; Sanz, Juana María; Zurlo, Amedeo; Fellin, Renato; Zuliani, Giovanni

doi:10.1093/gerona/glu028

Cited by 60 publications

(44 citation statements)

References 70 publications

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“…A recent cohort study showed that high glucose levels may be a risk factor for dementia and that the combination of DM2 and hypertension greatly increase the risk of cognitive impairment. Beside vascular factors, other risk factors include the formation of advanced glycosylation products, oxidative inflammation and stress, alterations in the hypothalamic-pituitary-adrenal axis and cortisol levels[30], and abnormalities in insulin secretion and signaling that promote cerebral amyloidosis.…”

Section: Discussionmentioning

confidence: 99%

Brain-derived neurotrophic factor plasma levels and premature cognitive impairment/dementia in type 2 diabetes

Ortíz¹,

Ramı́rez-Emiliano²,

Ramos-Rodríguez³

et al. 2016

WJD

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AIMTo assess the relationship of brain-derived neurotrophic factor (BDNF) with cognitive impairment in patients with type 2 diabetes.METHODSThe study included 40 patients with diabetes mellitus type 2 (DM2), 37 patients with chronic kidney disease in hem dialysis hemodialysis therapy (HD) and 40 healthy subjects. BDNF in serum was quantified by ELISA. The Folstein Mini-Mental State Examination was used to evaluate cognitive impairment.RESULTSThe patients with DM2 and the patients in HD were categorized into two groups, with cognitive impairment and without cognitive impairment. The levels of BDNF showed significant differences between patients with DM2 (43.78 ± 9.05 vs 31.55 ± 10.24, P = 0.005). There were no differences between patients in HD (11.39 ± 8.87 vs 11.11 ± 10.64 P = 0.77); interestingly, ferritin levels were higher in patients with cognitive impairment (1564 ± 1335 vs 664 ± 484 P = 0.001). The comparison of BDNF values, using a Kruskal Wallis test, between patients with DM2, in HD and healthy controls showed statistical differences (P < 0.001).CONCLUSIONLow levels of BDNF are associated with cognitive impairment in patients with DM2. The decrease of BDNF occurs early and progressively in patients in HD.

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Section: Discussionmentioning

confidence: 99%

Brain-derived neurotrophic factor plasma levels and premature cognitive impairment/dementia in type 2 diabetes

Ortíz¹,

Ramı́rez-Emiliano²,

Ramos-Rodríguez³

et al. 2016

WJD

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“…Brain-derived neurotrophic factor (BDNF) has antidiabetic properties, and reduced circulating BDNF is linked to dementia (Passaro et al, 2015). In the elderly, there may be a synergistic effect of cognitive decline and diabetes on reducing BDNF levels (Passaro et al, 2015).…”

Section: Osa Upregulates Glucosementioning

confidence: 99%

Evidence of neurodegeneration in obstructive sleep apnea: Relationship between obstructive sleep apnea and cognitive dysfunction in the elderly

Daulatzai

2015

J of Neuroscience Research

165

133

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The incidence of dementia and obstructive sleep apnea (OSA) increases with age. Late-onset Alzheimer's disease (AD) is an irreversible neurodegenerative disease of the elderly characterized by amyloid β (Aβ) plaques and neurofibrillary tangles. The disease involves widespread synaptic loss in the neocortex and the hippocampus. Rodent and clinical studies suggest that OSA impairs the structural integrity of several brain regions, including the medial temporal lobe. Indeed, hypoxia, hypertension, hypoperfusion, endothelial dysfunction, inflammation, and oxidative stress noted in OSA patients also occur in AD patients. This Review highlights pathological commonality, showing that OSA upregulates Aβ, tau hyperphosphorylation, and synaptic dysfunction. Indeed, OSA and hypertension trigger hypoperfusion and hypometabolism of brain regions, including cortex and hippocampus. Several studies show that hypertension-driven brain damage and pathogenic mechanisms lead to an Aβ increase. The pathophysiological mechanism by which OSA enhances hypertension may be linked to sympathoexcitation, oxidative stress, and endothelial dysfunction. Strong pathophysiological similarities that exist between OSA and AD are underscored here. For example, the hippocampus is negatively impacted in both OSA and AD. OSA promotes hippocampal atrophy, which is associated with memory impairment. Cognitive impairment, even in the absence of manifest dementia, is an important independent predictor of mortality. However, several pathophysiological mechanisms in OSA are reversible with appropriate therapy. OSA, therefore, is a modifiable risk factor of cognitive dysfunction, and treating OSA prior to mild cognitive impairment may be an effective prevention strategy to reduce risk for cognitive decline and AD in middle-aged persons and the elderly.

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“…Crossing bi-directionally the blood-brain barrier, BDNF can act at a systemic level. Low levels of plasma BDNF have been associated with dementia [10, 11], diabetes [11–13], depression [14, 15] and coronary syndrome [16]. …”

Section: Introductionmentioning

confidence: 99%

Computerized cognitive training and brain derived neurotrophic factor during bed rest: mechanisms to protect individual during acute stress

Passaro

Soavi

Marušič

et al. 2017

Aging

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Acute stress, as bed rest, was shown to increase plasma level of the neurotrophin brain-derived neurotrophic factor (BDNF) in older, but not in young adults. This increase might represent a protective mechanism towards acute insults in aging subjects. Since computerized cognitive training (CCT) is known to protect brain, herein we evaluated the effect of CCT during bed rest on BDNF, muscle mass, neuromuscular function and metabolic parameters. The subjects that underwent CCT did not show an increase of BDNF after bed rest, and showed an anti-insular modification pattern in metabolism. Neuromuscular function parameters, already shown to beneficiate from CCT, negatively correlated with BDNF in research participants undergoing CCT, while positively correlated in the control group. In conclusion, BDNF increase can be interpreted as a standardized protective mechanism taking place whenever an insult occurs; it gives low, but consistent preservation of neuromuscular function. CCT, acting as an external protective mechanism, seems to modify this standardized response, avoiding BDNF increase or possibly modifying its time course. Our results suggest the possibility of differential neuroprotective mechanisms among ill and healthy individuals, and the importance of timing in determining the effects of protective mechanisms.

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Brain-Derived Neurotrophic Factor Plasma Levels: Relationship With Dementia and Diabetes in the Elderly Population

Cited by 60 publications

References 70 publications

Brain-derived neurotrophic factor plasma levels and premature cognitive impairment/dementia in type 2 diabetes

Brain-derived neurotrophic factor plasma levels and premature cognitive impairment/dementia in type 2 diabetes

Evidence of neurodegeneration in obstructive sleep apnea: Relationship between obstructive sleep apnea and cognitive dysfunction in the elderly

Computerized cognitive training and brain derived neurotrophic factor during bed rest: mechanisms to protect individual during acute stress

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