Adult Neurogenesis in Neurodegenerative Diseases: Figure 1.

Winner, Beate; Winkler, Jürgen

doi:10.1101/cshperspect.a021287

Cited by 270 publications

(232 citation statements)

References 116 publications

Supporting

Mentioning

222

Contrasting

Unclassified

Order By: Relevance

“…While only few and conflicting studies about the extent of adult hippocampal neurogenesis in human AD patients are available (reviewed in ref. 11 ), numerous reports on the involvement of neurogenesis in transgenic AD mouse models have been published in recent years.…”

Section: Introductionmentioning

confidence: 99%

Altered neurogenesis in mouse models of Alzheimer disease

Wirths

2017

Neurogenesis

View full text Add to dashboard Cite

Amyloid-b (Ab) peptides, as well as a variety of other protein fragments, are derived from proteolytical cleavage of the amyloid precursor protein (APP) and have been demonstrated to play a key role in the pathological changes underlying Alzheimer disease (AD). In AD mouse models, altered neurogenesis has been repeatedly reported to be associated with further AD-typical pathological hallmarks such as extracellular plaque deposition, behavioral deficits or neuroinflammation. While a toxic role of Ab in neurodegeneration and impaired neuronal progenitor proliferation is likely and well-accepted, recent findings also suggest an important influence of APP-derived proteolitical fragments like the APP intracellular domain (AICD), as well as of APP itself.

show abstract

Section: Introductionmentioning

confidence: 99%

Altered neurogenesis in mouse models of Alzheimer disease

Wirths

2017

Neurogenesis

View full text Add to dashboard Cite

show abstract

“…Adult neurogenesis in the SGZ is thought to provide neural plasticity involved in hippocampal-dependent learning and memory [2] . The impairment of adult neurogenesis is involved in aging and neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD) [3] . However, the regulation of neurogenesis is unclear and the mechanisms need to be understood.…”

Section: Introductionmentioning

confidence: 99%

Aquaporin-4 Mediates the Suppressive Effect of Lipopolysaccharide on Hippocampal Neurogenesis

Liang

Yong

Huang

et al. 2016

Neuroimmunomodulation

View full text Add to dashboard Cite

Objective: Aquaporin-4 (AQP4), a key molecule for water homeostasis in the brain, is associated with adult neurogenesis, but its mechanisms regulating adult neural stem cells (aNSC) remain largely unexplored. Neuroinflammation has a relevant influence on adult neurogenesis, which is a common feature in various neurodegenerative diseases. Considering the possible link between neuroinflammation and AQP4, we speculate that AQP4 may mediate the synthesis and release of proinflammatory cytokines in glia and then indirectly regulate adult hippocampal neurogenesis. Methods: Using AQP4 knockout mice, we investigated the effects of AQP4 on hippocampal neurogenesis after lipopolysaccharide (LPS)-induced neuroinflammation. Results: We unexpectedly found that AQP4 deficiency attenuated the decrease in aNSC proliferation after systemic LPS exposure, accompanied by inhibition of glial activation and suppression of the production of proinflammatory cytokines in the hippocampus. Meanwhile, in vivo studies demonstrated that LPS-induced activated microglia did not express AQP4, indicating the impossibility of direct regulation of AQP4 to activate microglia. Furthermore, we demonstrated in vitro that AQP4 deficiency inhibited astrocyte activation and reduced the release of proinflammatory cytokines from astrocytes. Conclusion: Our data suggest that AQP4 mediates the suppressive effect of neuroinflammation on hippocampal neurogenesis via regulation of the astroglial response.

show abstract

“…Therefore, it has been suggested that altered AN in the hippocampus plays a role in the etiopathology of neurodegenerative disorders such as AD (for review, see Winner and Winkler 2015) and vascular dementia (Ekonomou et al 2011). Cerebrovascular functions and AN both decline during aging (Kalaria 2009;Kempermann 2015) which stands to reason as AN occurs within an angiogenic niche (Palmer et al 2000).…”

Section: Future Strategiesmentioning

confidence: 99%

The diabetic brain and cognition

et al. 2017

View full text Add to dashboard Cite

The prevalence of both Alzheimer's disease (AD) and vascular dementia (VaD) is increasing with the aging of the population. Studies from the last several years have shown that people with diabetes have an increased risk for dementia and cognitive impairment. Therefore, the authors of this consensus review tried to elaborate on the role of diabetes, especially diabetes type 2 (T2DM) in both AD and VaD. Based on the clinical and experimental work of scientists from 18 countries participating in the International Congress on Vascular Disorders and on literature search using PUBMED, it can be concluded that T2DM is a risk factor for both, AD and VaD, based on a pathology of glucose utilization. This pathology is the consequence of a disturbance of insulin-related mechanisms leading to brain insulin resistance. Although the underlying pathological mechanisms for AD and VaD are different in many aspects, the contribution of T2DM and insulin resistant brain state (IRBS) to cerebrovascular disturbances in both disorders

show abstract

Adult Neurogenesis in Neurodegenerative Diseases: Figure 1.

Cited by 270 publications

References 116 publications

Altered neurogenesis in mouse models of Alzheimer disease

Altered neurogenesis in mouse models of Alzheimer disease

Aquaporin-4 Mediates the Suppressive Effect of Lipopolysaccharide on Hippocampal Neurogenesis

The diabetic brain and cognition

Contact Info

Product

Resources

About