New Insights on the Effects of Krill Oil Supplementation, a High-Fat Diet, and Aging on Hippocampal-Dependent Memory, Neuroinflammation, Synaptic Density, and Neurogenesis.

Krill oil (KO) has been described as having the potential to ameliorate the detrimental consequences of a high-fat diet (HFD) on the aging brain, though the magnitude and mechanism of this benefit is unclear. We thus hypothesized that dietary KO supplementation could counteract the effects of cognitive aging and an HFD on spatial learning, neuroinflammation, neurogenesis, and synaptic density in the cortex and hippocampus of aged rats. Sixteen-month-old Sprague Dawley rats were fed for 12 weeks while being divided into four groups: control (CON); control with KO supplementation (CONKO); high-fat diet (HF); and high-fat diet with KO supplementation (HFKO).

Can krill oil be of use for counteracting neuroinflammatory processes induced by high fat diet and aging?

Most neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, demonstrate preceding or on-going inflammatory processes. Therefore, discovering effective means of counteracting detrimental inflammatory mediators in the brain could help alter aging-related disease onset and progression. Fish oil and marine-derived omega-3, long-chain polyunsaturated fatty acids (LC n-3) have shown promising anti-inflammatory effects both systemically and centrally.

p35 Hemizygous Deletion in 5xFAD Mice Increases Aβ Plaque Load in Males but Not in Females.

Increased amyloid beta (Aβ) deposition is implicated in early stages of Alzheimer's disease (AD). Although aberrant Cdk5 activity mediated by Cdk5/p25 is suggested to promote Aβ plaque deposition, the effects of Cdk5 inhibition on Aβ plaque loads in AD mouse models have been equivocal, possibly due to the fact that Cdk5 can be activated by p35 or p39 and their cleaved products. Here we evaluated the effect of p35 knockdown on Aβ plaque formation by constitutively knocking out a single p35 allele in 5xFAD mice.

Potential Therapeutical Contributions of the Endocannabinoid System towards Aging and Alzheimer's Disease.

Aging can lead to decline in cognition, notably due to neurodegenerative processes overwhelming the brain over time. As people live longer, numerous concerns are rightfully raised toward long-term slowly incapacitating diseases with no cure, such as Alzheimer's disease. Since the early 2000's, the role of neuroinflammation has been scrutinized for its potential role in the development of diverse neurodegenerative diseases notably because of its slow onset and chronic nature in aging.

MT5-MMP is a new pro-amyloidogenic proteinase that promotes amyloid pathology and cognitive decline in a transgenic mouse model of Alzheimer's disease.

Membrane-type 5-matrix metalloproteinase (MT5-MMP) is a proteinase mainly expressed in the nervous system with emerging roles in brain pathophysiology. The implication of MT5-MMP in Alzheimer's disease (AD), notably its interplay with the amyloidogenic process, remains elusive. Accordingly, we crossed the genetically engineered 5xFAD mouse model of AD with MT5-MMP-deficient mice and examined the impact of MT5-MMP deficiency in bigenic 5xFAD/MT5-MMP(-/-) mice.