The neurotoxicology of hard foraging and fat-melts

Finch, Caleb E.

doi:10.1073/pnas.0408437101

Cited by 8 publications

(5 citation statements)

References 33 publications

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“…Consistent with the observation that caloric restriction attenuates MPTP-induced depletion of dopamine, the distance moved and speed of movement increased more than two-fold in caloric restricted monkeys compared with those on control diet (Maswood et al, 2004). From an evolutionary point of view, and based on experimental data, it was speculated that the neuroprotective effects of caloric restriction could be due to the induction of growth factors by increased motor activity (Finch, 2004). In fact, activation of the same cellular and molecular pathways that occur in response to mild dietary restriction and intermittent fasting-induced stress can occur in response to physical exercise and cognitive stimulation (Mattson et al, 2004).…”

Section: Is There a Gdnf Diet?supporting

confidence: 61%

Towards New Therapies for Parkinson's Disease

Finkelstein¹

2011

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He is a full time researcher that gives specialist undergraduate and postgraduate lectures in neurobiology and anatomy to science, medical and physiotherapy students. His research investigates the neurobiology on neurodegeneration with particular emphasis on the processes that occur during Parkinson's Disease. He has produced around 100 publications in refereed journals as well as numerous book chapters and international conference presentations. He is a scientific consultant for two biotechnology companies producing and developing novel small molecules for the treatment of neurodegenerative diseases (Parkinson's, Alzheimer's and Huntington's Diseases). He is an editor and a reviewer for many international journals and granting bodies.

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Section: Is There a Gdnf Diet?supporting

confidence: 61%

Towards New Therapies for Parkinson's Disease

Finkelstein¹

2011

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Section: Is There a Gdnf Diet?supporting

confidence: 53%

GDNF and PD: Less Common Points of View

Saavedra¹,

Baltazar²

2011

Towards New Therapies for Parkinson's Disease

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“…That a reduction in CORT in DR models would be additionally beneficial to hippocampal neurons was postulated by Finch (2004). Recent studies appear to provide support for this hypothesis.…”

Section: Discussionmentioning

confidence: 93%

Neuroprotection provided by dietary restriction in rats is further enhanced by reducing glucocortocoids

Qiu

Spangler

Wan

et al. 2012

Neurobiology of Aging

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Glucocorticoids (GC)--corticosterone (CORT) in rodents and cortisol in primates--are stress-induced hormones secreted by adrenal glands that interact with the hypothalamic pituitary axis. High levels of cortisol in humans are observed in neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD), as well as in diabetes, post-traumatic stress syndrome, and major depression. Experimental models of diabetes in rats and mice have demonstrated that reduction of CORT reduces learning and memory deficits and attenuates loss of neuronal viability and plasticity. In contrast to the negative associations of elevated GC levels, CORT is moderately elevated in dietary restriction (DR) paradigms which are associated with many healthy anti-aging effects including neuroprotection. We demonstrate here in rats that ablating CORT by adrenalectomy (ADX) with replenishment to relatively low levels (30% below that of controls) prior to the onset of a DR regimen (ADX-DR) followed by central administration of the neurotoxin, kainic acid (KA), significantly attenuates learning deficits in a 14-unit T-maze task. The performance of the ADX-DR KA group did not differ from a control group (CON) that did not receive KA and was fed ad libitum (AL). By contrast, the sham-operated DR (SHAM-DR KA) group, SHAM-AL KA group, and ADX-AL KA group demonstrated poorer learning behavior in this task compared to the CON group. Stereological analysis revealed equivalent DR-induced neuroprotection in the SH-DR KA and ADX-DR KA groups, as measured by cell loss in the CA2/CA3 region of the hippocampus, while substantial cell loss was observed in SH-AL and ADX-AL rats. A separate set of experiments was conducted with similar dietary and surgical treatment conditions but without KA administration to examine markers of neurotrophic activity, brain-derived neurotrophic factor (BDNF), transcriptions factors (pCREB), and chaperone proteins (HSP-70). Under these conditions, we noted elevations in both BDNF and pCREB in ADX DR rats compared to the other groups; whereas, HSP-70, was equivalently elevated in ADX-DR and SH-DR groups and was higher than observed in both SH-AL and ADX-AL groups. These results support findings that DR protects hippocampal neurons against KA-induced cellular insult. However, this neuroprotective effect was further enhanced in rats with a lower-than control level of CORT resulting from ADX and maintained by exogenous CORT supplementation. Our results then suggest that DR-induced physiological elevation of GC may have negative functional consequences to DR-induced beneficial effects. These negative effects, however, can be compensated by other DR-produced cellular and molecular protective mechanisms.

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The neurotoxicology of hard foraging and fat-melts

Cited by 8 publications

References 33 publications

Towards New Therapies for Parkinson's Disease

Towards New Therapies for Parkinson's Disease

GDNF and PD: Less Common Points of View

Neuroprotection provided by dietary restriction in rats is further enhanced by reducing glucocortocoids

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