Quantitation of BDNF mRNA in human parietal cortex by competitive reverse transcription-polymerase chain reaction: decreased levels in Alzheimer's disease

Holsinger, R. M. Damian; Schnarr, Jane; Henry, Pauline; Castelo, Vivian T; Fahnestock, Margaret

doi:10.1016/s0169-328x(00)00023-1

Cited by 296 publications

(198 citation statements)

References 41 publications

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“…63 BDNF is also found in lower than normal levels in the AD brain. [64][65][66] Adlard et al 59 examined the effect of wheel running on BDNF levels in rat models, and observed a positive dose response between such physical activity and cerebral BDNF levels. Furthermore, in the presence of oestrogen, physical activity was able to increase levels of hippocampal BDNF mRNA in female rats.…”

Section: Exercise May Increase Levels Of Growth Factors and Neurotranmentioning

confidence: 99%

Multiple effects of physical activity on molecular and cognitive signs of brain aging: can exercise slow neurodegeneration and delay Alzheimer’s disease?

2012

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Western countries are experiencing aging populations and increased longevity; thus the incidence of dementia and Alzheimer's disease (AD) in these countries is projected to soar.In the absence of a therapeutic drug, non-pharmacological preventative approaches are being investigated. One of these approaches is regular participation in physical activity or exercise.This paper reviews studies that have explored the relationship between physical activity and cognitive function, cognitive decline, AD/dementia risk and AD-associated biomarkers and processes. There is now strong evidence that links regular physical activity or exercise to higher cognitive function, decreased cognitive decline and reduced risk of AD or dementia.Nevertheless, these associations require further investigation, more specifically with interventional studies that include long follow-up periods. In particular, relatively little is known about the underlying mechanism(s) of the associations between physical activity and AD neuropathology; clearly this is an area in need of further research, particularly in human populations. While benefits of physical activity or exercise are clearly recognised, there is a need to clarify how much physical activity provides the greatest benefit and also whether people of different genotypes require tailored exercise regimes.3

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Section: Exercise May Increase Levels Of Growth Factors and Neurotranmentioning

confidence: 99%

Multiple effects of physical activity on molecular and cognitive signs of brain aging: can exercise slow neurodegeneration and delay Alzheimer’s disease?

2012

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“…Transgenic mice with reduced BDNF levels exhibit defects in synaptic transmission, LTP, and memory tests that are rescued by exogenous BDNF administration (Korte et al, 1995;Patterson et al, 1996;Olofsdotter et al, 2000). BDNF mRNA and protein are significantly decreased in AD and mildly cognitive impaired (MCI) subjects compared with controls (Phillips et al, 1991;Connor et al, 1997;Ferrer et al, 1999;Hock et al, 2000;Holsinger et al, 2000). Moreover, the decrease in BDNF correlates with the severity of cognitive impairment (Peng et al, 2005), identifying BDNF downregulation as an early and possibly underlying event in AD.…”

Section: Introductionmentioning

confidence: 99%

Oligomeric Amyloid Decreases Basal Levels of Brain-Derived Neurotrophic factor (BDNF) mRNA via Specific Downregulation of BDNF Transcripts IV and V in Differentiated Human Neuroblastoma Cells

Garzon¹,

Fahnestock²

2007

J. Neurosci.

171

127

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Alzheimer's disease (AD) is a senile dementia characterized by amyloid plaques, neurofibrillary tangles, and synaptic and cell loss. The "amyloid cascade" hypothesis suggests that amyloid-␤ (A␤), the peptide deposited as amyloid plaques, is the primary insult in AD. However, debate continues over the mechanism of A␤ toxicity and whether fibrillar or oligomeric A␤ is the active species of the peptide that ultimately causes the synaptic loss and dementia associated with AD. Brain-derived neurotrophic factor (BDNF) is required for survival and function of cells compromised in AD. Decreased BDNF causes defects in long-term potentiation and memory and correlates with cognitive decline. We previously demonstrated that BDNF reduction occurs early in the course of AD, suggesting that decreased BDNF may promote neuronal dysfunction in AD. We also demonstrated that three of seven human BDNF transcripts are specifically downregulated in AD. What pathological feature(s) of AD leads to the decreased BDNF is unknown.In this study, we administered both fibrillar and oligomeric conformations of A␤ 1-42 to differentiated SH-SY5Y, a human neuroblastoma cell line, and measured both phosphorylated cAMP response element-binding protein (CREB), a regulator of BDNF transcription, and BDNF total mRNA. We found that oligomeric but not fibrillar preparations of A␤ 1-42 significantly decrease both phosphorylated CREB and total BDNF mRNA. Furthermore, oligomeric A␤ 1-42 decreases BDNF transcripts IV and V in these cells, demonstrating that A␤ 1-42 downregulates the major BDNF transcript decreased in vivo in the AD brain. Thus, oligomeric A␤ 1-42 could compromise neuronal function, causing memory loss and cognitive dysfunction by downregulation of BDNF in AD.

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“…Recent studies implicate both genetic (Piccini et al 1999;Sveinbjornsdottir et al 2000) and environmental (Schapira 1997) factors in the pathogenesis of PD. The brain-derived neurotrophic factor (BDNF) gene encodes a nerve growth factor, and is highly expressed in the nervous system (Holsinger et al 2000;Murer et al 2001). Since BDNF promotes the survival of dopaminergic neurons in the substantia nigra, and expression of BDNF is reduced in PD substantia nigra, it seems that a genetic variation in BDNF, e.g.…”

Section: Introductionmentioning

confidence: 99%

The role of G196A polymorphism in the brain-derived neurotrophic factor gene in the cause of Parkinson’s disease: a meta-analysis

Ζιντζαράς

Hadjigeorgiou

2005

J Hum Genet

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The association between Parkinson's disease (PD) and the G196A polymorphism in the brain-derived neurotrophic factor (BDNF) gene has been investigated in several case-control studies, producing contradictory results: one study indicated that homozygocity of AA is associated with PD, another study produced the opposite result, whereas other studies found no association. To investigate these contradictory findings, a metaanalysis of all available association studies between the G196A polymorphism and the risk of developing PD was conducted. Four out of six identified studies included populations of East Asian descent, and two included populations of European descent (Whites). Overall, the meta-analysis of the allele contrast (A vs G) suggested large heterogeneity between studies (P=0.07, I 2 =51%) and no association between G196A and the risk of developing PD: random effects odds ratio (OR)=1.00 [95% CI (0.85, 1.18)]. The sensitivity analysis (exclusion of two studies: one East Asian and one White) with the controls not in Hardy-Weinberg equilibrium showed large heterogeneity (P=0.10, I 2 =52%) and no significant association: random effects OR=0.94 [95% CI (0.77, 1.15)]. The subgroup analyses for East Asians and Whites produced no significant association. In addition, the contrast of homozygotes, and the dominant and recessive models for allele A did not support a major role for this polymorphism in the pathogenesis of PD. There were no sources of bias in the selected studies, and the differential magnitude of effect in large vs small studies was not significant. The metaanalysis results suggest that the involvement of the BDNF gene in susceptibility to PD merits further exploration with larger and more rigorous population association studies.

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Quantitation of BDNF mRNA in human parietal cortex by competitive reverse transcription-polymerase chain reaction: decreased levels in Alzheimer's disease

Cited by 296 publications

References 41 publications

Multiple effects of physical activity on molecular and cognitive signs of brain aging: can exercise slow neurodegeneration and delay Alzheimer’s disease?

Multiple effects of physical activity on molecular and cognitive signs of brain aging: can exercise slow neurodegeneration and delay Alzheimer’s disease?

Oligomeric Amyloid Decreases Basal Levels of Brain-Derived Neurotrophic factor (BDNF) mRNA via Specific Downregulation of BDNF Transcripts IV and V in Differentiated Human Neuroblastoma Cells

The role of G196A polymorphism in the brain-derived neurotrophic factor gene in the cause of Parkinson’s disease: a meta-analysis

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