Plasma levels of BDNF and EGF are reduced in acute stroke patients.

Stroke affects almost 14 million people worldwide each year. It is the second leading cause of death and a major cause of acquired disability. The degree of initial impairment in cognitive and motor functions greatly affects the recovery, but idiosyncratic factors also contribute. These are largely unidentified, which contributes to making accurate prediction of recovery challenging. Release of soluble regulators of neurotoxicity, neuroprotection and repair are presumably essential. Here we measured plasma levels of known regulators of neuroprotection and repair in patients with mild acute ischemic stroke and compared them to the plasma levels in healthy age and gender matched controls. We found that the levels of BDNF and EGF were substantially lower in stroke patients than in healthy controls, while the levels of bFGF and irisin did not differ between the groups. The lower levels of growth factors highlight that during the acute phase of stroke, there is a mismatch between the need for neuroprotection and repair, and the brain's ability to induce these processes. Large individual differences in growth factor levels were seen among the stroke patients, but whether these can be used as predictors of long-term prognosis remains to be investigated.

L-lactate induces neurogenesis in the mouse ventricular-subventricular zone via the lactate receptor HCA1.

AIM: Adult neurogenesis occurs in two major niches in the brain: the subgranular zone of the hippocampal formation and the ventricular-subventricular zone. Neurogenesis in both niches is reduced in ageing and neurological disease involving dementia. Exercise can rescue memory by enhancing hippocampal neurogenesis, but whether exercise affects adult neurogenesis in the ventricular-subventricular zone remains unresolved. Previously, we reported that exercise induces angiogenesis through activation of the lactate receptor HCA1. The aim of the present study is to investigate HCA1 -dependent effects on neurogenesis in the two main neurogenic niches. METHODS: Wild-type and HCA1 knock-out mice received high intensity interval exercise, subcutaneous injections of L-lactate, or saline injections, five days per week for seven weeks. Well-established markers for proliferating cells (Ki-67) and immature neurons (doublecortin), were used to investigate neurogenesis in the subgranular zone and the ventricular-subventricular zone. RESULTS: We demonstrated that neurogenesis in the ventricular-subventricular zone is enhanced by HCA1 activation: Treatment with exercise or lactate resulted in increased neurogenesis in wild-type, but not in HCA1 knock-out mice. In the subgranular zone, neurogenesis was induced by exercise in both genotypes, but unaffected by lactate treatment. CONCLUSION: Our study demonstrates that neurogenesis in the two main neurogenic niches in the brain is regulated differently: Neurogenesis in both niches was induced by exercise, but only in the ventricular-subventricular zone was neurogenesis induced by lactate through HCA1 activation. This opens for a role of HCA1 in the physiological control of neurogenesis, and potentially in counteracting age-related cognitive decline.