Environmental Enrichment Counteracts Alzheimer’s Neurovascular Dysfunction in TgCRND8 Mice

Herring, Arne; Yasin, Hamzah; Ambrée, Oliver; Sachser, Norbert; Paulus, Werner; Keyvani, Kathy

doi:10.1111/j.1750-3639.2007.00094.x

Cited by 70 publications

(58 citation statements)

References 40 publications

(51 reference statements)

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“…Available treatments amount to several drugs that provide temporary relief or slow progression (Sparks et al 2005;Kehoe and Wilcock 2007;Relkin et al 2009). Risk of AD may be reduced, however, by antioxidants (Grundman and Denaney 2002;Holmquist et al 2007;Cole and Frautschy 2010), healthy diets (Gu et al 2010), environmental enrichment (Jankowski et al 2005;Herring et al 2008), and exercise (Adlard et al 2005). Preservation of cognitive function into older ages is associated with increased longevity (Barzilai et al 2006).…”

Section: Introductionmentioning

confidence: 99%

“…Neurobiological and behavioral manifestations of cognitive decline relevant to humans are shared by several animal models (Gallagher and Nicolle 1993) including those genetically engineered to express attributes of human pathologies such AD (e.g., Adlard et al 2005;Jankowski et al 2005;Herring et al 2008). Aging rodents are also especially vulnerable to declining spatial memory (Foster 1999), and this can be quantified by performance in the Morris water maze (MWM) (Brandies et al 1989;Gallagher and Burwell 1989;Wehner and Silva 1996;Crawley et al 1997;Adlard et al 2005;Jankowski et al 2005).…”

Section: Introductionmentioning

confidence: 99%

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A complex dietary supplement augments spatial learning, brain mass, and mitochondrial electron transport chain activity in aging mice

Aksenov

Long

Liu

et al. 2011

AGE

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We developed a complex dietary supplement designed to offset five key mechanisms of aging and tested its effectiveness in ameliorating age-related cognitive decline using a visually cued Morris water maze test. All younger mice (<1 year old) learned the task well. However, older untreated mice (>1 year) were unable to learn the maze even after 5 days, indicative of strong cognitive decline at older ages. In contrast, no cognitive decline was evident in older supplemented mice, even when ∼2 years old. Supplemented older mice were nearly 50% better at locating the platform than age-matched controls. Brain weights of supplemented mice were significantly greater than controls, even at younger ages. Reversal of cognitive decline in activity of complexes III and IV by supplementation was significantly associated with cognitive improvement, implicating energy supply as one possible mechanism. These results represent proof of principle that complex dietary supplements can provide powerful benefits for cognitive function and brain aging.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A complex dietary supplement augments spatial learning, brain mass, and mitochondrial electron transport chain activity in aging mice

Aksenov

Long

Liu

et al. 2011

AGE

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“…185,191,195 Moreover, EE increases angiogenesis and facilitates blood Ab clearance through a differential regulation of Ab receptor/transporter molecules in TgCRND8 mice. 196 Lazarov et al 189 carried out a microarray analysis to identify gene expression changes in APP/PS1 transgenic mice placed in EE conditions. This study revealed a total of 41 genes differentially regulated in response to EE, with the vast majority of genes that showed elevated expression encoding polypeptides involved in learning and memory, synaptic plasticity, neurogenesis, vasculogenesis, neuronal cell growth and cell survival pathways (e.g., NGF-1A, BDNF; CaMKIIa).…”

Section: Impact Of Ee On the Brain L Baroncelli Et Almentioning

confidence: 99%

Nurturing brain plasticity: impact of environmental enrichment

et al. 2009

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Environmental enrichment (EE) is known to profoundly affect the central nervous system (CNS) at the functional, anatomical and molecular level, both during the critical period and during adulthood. Recent studies focusing on the visual system have shown that these effects are associated with the recruitment of previously unsuspected neural plasticity processes. At early stages of brain development, EE triggers a marked acceleration in the maturation of the visual system, with maternal behaviour acting as a fundamental mediator of the enriched experience in both the foetus and the newborn. In adult brain, EE enhances plasticity in the cerebral cortex, allowing the recovery of visual functions in amblyopic animals. The molecular substrate of the effects of EE on brain plasticity is multi-factorial, with reduced intracerebral inhibition, enhanced neurotrophin expression and epigenetic changes at the level of chromatin structure. These findings shed new light on the potential of EE as a non-invasive strategy to ameliorate deficits in the development of the CNS and to treat neurological disorders.

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“…In a previous AD animal model study, the authors observed an increase in RAGE but a decrease in LRP1 at the BBB (Herring et al, 2008). Other studies reported that decreased LRP1 and increased RAGE were involved in Aβ uptake in a BBB cell model using a rat brain endothelial cell line (Yamada et al, 2008;Kim et al, 2013a).…”

Section: Discussionmentioning

confidence: 87%

Mercury-induced amyloid-beta (Aβ) accumulation in the brain is mediated by disruption of Aβ transport

2014

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-According to a recent study, mercury (Hg) exposure contributes to Alzheimer's disease (AD). However, the underlying mechanisms are not understood. This study investigated the effect of methylmercury (MeHg) treatment on the generation, degradation, and transport of amyloid β-protein (Aβ) in the brain. Wistar rats were administered MeHg by gavage (0, 20, 200, and 2,000 μg Hg/kg/day) for 4 weeks. The total Hg in the blood and brain regions was measured, and the levels of Aβ 42 in plasma, cerebrospinal fluid (CSF), and brain regions were estimated. The expression of amyloid precursor protein (APP), beta-site APP-cleaving enzyme 1 (BACE1), and neprilysin (NEP) in the brain regions was determined, in addition to the expression of low-density lipoprotein receptor-related protein 1 (LRP1) and the receptor for advanced glycation end products (RAGE) in the brain capillary endothelium (BCE). Finally, the amount of soluble low-density lipoprotein receptor-related protein (sLRP) in the plasma was determined. Aβ 42 levels were decreased in the CSF of the 2,000 μg Hg/kg/day group compared with controls, and Aβ 42 levels increased in the hippocampus (HC) in a dose-dependent manner. MeHg decreased LRP1 expression but increased RAGE levels in BCE. sLRP levels were decreased in the plasma of the MeHgtreated rats. They were positively correlated with CSF Aβ 42 and negatively correlated with Aβ 42 and Hg levels in HC. These results imply that MeHg reduces the transportation of Aβ, thereby resulting in the accumulation of the protein in the HC. Plasma sLRP levels may be an early biomarker of Hg-induced Aβ accumulation in the brain.

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Environmental Enrichment Counteracts Alzheimer’s Neurovascular Dysfunction in TgCRND8 Mice

Cited by 70 publications

References 40 publications

A complex dietary supplement augments spatial learning, brain mass, and mitochondrial electron transport chain activity in aging mice

A complex dietary supplement augments spatial learning, brain mass, and mitochondrial electron transport chain activity in aging mice

Nurturing brain plasticity: impact of environmental enrichment

Mercury-induced amyloid-beta (Aβ) accumulation in the brain is mediated by disruption of Aβ transport

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