The role of adult hippocampal neurogenesis in brain health and disease

Toda, Tatsuki; Parylak, Sarah; Linker, Sara B.; Gage, Fred H.

doi:10.1038/s41380-018-0036-2

Cited by 486 publications

(412 citation statements)

References 290 publications

(219 reference statements)

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“…(43–47) While this particular type of brain injury could not be detected even with prenatal MRI, it would be expected to correlate with the reported early onset of seizures/epilepsy in human infants, perturbations to later learning and memory development, and potentially even later onset depression and age-related cognitive decline. (48–50) A recent study in infant nonhuman primates also correlated ZIKV infection with hippocampal growth arrest, dysfunctional connectivity by functional MRI, and abnormal socioemotional processing. (51) Longitudinal studies are needed to understand the implications of ZIKV-associated injury to neurogenic cells in the fetus or young children and whether this injury might result in a predisposition to learning disorders, developmental delay or mental illness in childhood and adolescence.…”

Section: Broadening Spectrum Of Zikv-associated Fetal Injurymentioning

confidence: 99%

Zika virus and the nonmicrocephalic fetus: why we should still worry

Walker

Little²,

Roby

et al. 2019

American Journal of Obstetrics and Gynecology

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Zika virus (ZIKV) is a mosquito-transmitted flavivirus and was first linked to congenital microcephaly due to a large outbreak in Northeastern Brazil. Although the ZIKV epidemic is now in decline, pregnancies in large parts of the Americas remain at risk due to ongoing transmission and the potential for new outbreaks. This review presents why Zika virus is still a complex and worrisome public health problem with an expanding spectrum of birth defects and why ZIKV and related viruses may evade the immune response to injure the fetus. Recent reports indicate that the spectrum of fetal brain and other anomalies associated with ZIKV exposure is broader and more complex than microcephaly alone and includes subtle fetal brain and ocular injuries; thus, the ability to prenatally diagnose fetal injury associated with ZIKV infection remains limited. New studies indicate that ZIKV imparts disproportionate effects on fetal growth with an unusual femur-sparing profile, potentially providing a new approach to identify viral injury to the fetus. Studies to determine the limitations of prenatal and postnatal testing for detection of ZIKV-associated birth defects and long-term neurocognitive deficits are needed to better guide counseling for women with a possible infectious exposure. It is also imperative that we investigate why ZIKV is so adept at infecting the placenta and the fetal brain to better predict other viruses with similar capabilities that may give rise to new epidemics. The efficiency with which ZIKV evades the early immune response to enable infection of the mother, placenta and fetus is likely critical for understanding why the infection may either be fulminant or limited. Furthermore, studies suggest that several emerging and related viruses may also cause birth defects, including West Nile virus, which is endemic in many parts of the United States. With mosquito-borne diseases increasing worldwide, there remains an urgent need to better understand the pathogenesis of ZIKV and related viruses to protect pregnancies and child health.

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Section: Broadening Spectrum Of Zikv-associated Fetal Injurymentioning

confidence: 99%

Zika virus and the nonmicrocephalic fetus: why we should still worry

Walker

Little²,

Roby

et al. 2019

American Journal of Obstetrics and Gynecology

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“…Here, newly generated neurons are integrated into local circuitries, where they play a role in plasticity of the HC and olfactory system . Ageing and disease modify the neurogenic potential of the brain, with a general trend toward its decline . Impairment in neurogenesis is counteracted by a compensatory increase as observed in patients and in AD animal models.…”

Section: Neurogenesismentioning

confidence: 99%

Early compensatory responses against neuronal injury: A new therapeutic window of opportunity for Alzheimer's Disease?

2018

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Alzheimer's disease (AD) is characterized by extensive neurodegeneration and inflammation in selective brain areas, linked to severely disabling cognitive deficits. Before full manifestation, different stages appear with progressively increased brain pathology and cognitive impairment. This significantly extends the time lag between initial molecular triggers and appearance of detectable symptoms. Notably, a number of studies in the last decade have revealed that in the early stage of mild cognitive impairment, events that appear in contrast with neuronal distress may occur. These have been reproduced in vitro and in animal models and include increase in synaptic elements, increase in synaptic and metabolic activity, enhancement of neurotrophic milieu and changes in glial cell reactivity and inflammation. They have been interpreted as compensatory responses that could either delay disease progression or, in the long run, result detrimental. For this reason, these mechanisms define a new and previously undervalued window of opportunity for intervention. Their importance resides especially in their early appearance. Directing efforts to better characterize this stage, in order to identify new pharmacological targets, is an exciting new avenue to future advances in AD research.

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“…In other brain areas such as the hippocampus or the olfactory bulb, both decreased proliferation or excessive proliferation and subsequent depletion of the NSC pool results in a loss of adult neurogenesis [28, 29]. A loss of adult neurogenesis in the hippocampus and olfactory bulb has been linked to impairments in some of the functions in which these areas are involved [30, 31]. Similarly, inhibition of adult ME neurogenesis results in the impairment of some hypothalamic functions, i.e.…”

Section: Discussionmentioning

confidence: 99%

Early life stress decreases the proliferation and numbers of adult hypothalamic neural stem cells

Bielefeld

Abbink

Davidson

et al. 2019

Preprint

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Early life stress (ELS) is a potent environmental factor that can confer enduring effects on brain structure and function. Exposure to stress during early life has been linked to a wide range of physiopathological consequences later in life. In particular, ELS has been shown to have lasting effects on neurogenesis in the adult brain, suggesting that ELS is a significant regulator of adult neural stem cell function. Here, we investigated the effect of ELS on the numbers and proliferation of neural stem cells in the hypothalamus of adult mice.We show that ELS has long term negative effects on hypothalamic neural stem cell numbers and on their proliferation. Specifically, ELS reduced the total numbers of PCNA+ cells present in hypothalamic areas surrounding the 3 rd ventricle; the numbers of PCNA+/Sox2+/Nestin-GFP+ cells present in the medial eminence at the base of the 3 rd ventricle; and the number of β-tanycytes around the ventral 3rd ventricle, without affecting the numbers of α-tanycytes in more dorsal areas. These results suggest that a reduction of proliferation and tanycyte numbers contributes to the effects of ELS on the hypothalamus and its consequent physiological alterations. 7

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The role of adult hippocampal neurogenesis in brain health and disease

Cited by 486 publications

References 290 publications

Zika virus and the nonmicrocephalic fetus: why we should still worry

Zika virus and the nonmicrocephalic fetus: why we should still worry

Early compensatory responses against neuronal injury: A new therapeutic window of opportunity for Alzheimer's Disease?

Early life stress decreases the proliferation and numbers of adult hypothalamic neural stem cells

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