Cited by 161Neurogenesis and neuroplasticity mechanismsAlzheimer's disease research and treatmentsMemory and Neural Mechanisms

The DOI matches its Crossref record; 109 of the 109 references it cites were found in a registry or an index.

Alzheimer’s disease and hippocampal adult neurogenesis; exploring shared mechanisms

Open access
Hollands, Carolyn, Bartolotti, Nancy, Lazarov, Orly·2016·Frontiers in Neuroscience

Abstract

New neurons incorporate into the granular cell layer of the dentate gyrus throughout life. Neurogenesis is modulated by behavior and plays a major role in hippocampal plasticity. Along with older mature neurons, new neurons structure the dentate gyrus, and determine its function. Recent data suggest that the level of hippocampal neurogenesis is substantial in the human brain, suggesting that neurogenesis may have important implications for human cognition. In support of that, impaired neurogenesis compromises hippocampal function and plays a role in cognitive deficits in Alzheimer's disease mouse models. We review current work suggesting that neuronal differentiation is defective in Alzheimer's disease, leading to dysfunction of the dentate gyrus. Additionally, alterations in critical signals regulating neurogenesis, such as presenilin-1, Notch 1, soluble amyloid precursor protein, CREB, and β-catenin underlie dysfunctional neurogenesis in Alzheimer's disease. Lastly, we discuss the detectability of neurogenesis in the live mouse and human brain, as well as the therapeutic implications of enhancing neurogenesis for the treatment of cognitive deficits and Alzheimer's disease.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3389/fnins.2016.00178

Cites

109 of 109 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 Common mechanisms of neurogenesis and Alzheimer's disease and the implications for learning. (A) Signals that play a role in neurogenesis, such as Notch-1, Wnt/β-catenin, CREB, sAPP, tau, and presenilin-1 are implicated in Alzheimer's disease. (B) Following learning, changes in the neurogenic niche include alterations in Notch and sAPP, increased expression of neurotrophins such as VEGF, BDNF, and IGF which enhance angiogenesis and provide support for the neurogenic niche and lead to increased neurogenesis. Upregulation of CREB signaling by neural progenitor cells and neurons may promote survival and maturation of NPCs. Increased dendritic branching of mature neurons and synaptic plasticity may be mediated by presenilin-1 and APP. The factors mediating these processes are dysfunctional or compromised in Alzheimer's disease, suggesting that defective neurogenesis may affect hippocampal function in Alzheimer's disease.
Figure 1 Common mechanisms of neurogenesis and Alzheimer's disease and the implications for learning. (A) Signals that play a role in neurogenesis, such as Notch-1, Wnt/β-catenin, CREB, sAPP, tau, and presenilin-1 are implicated in Alzheimer's disease. (B) Following learning, changes in the neurogenic niche include alterations in Notch and sAPP, increased expression of neurotrophins such as VEGF, BDNF, and IGF which enhance angiogenesis and provide support for the neurogenic niche and lead to increased neurogenesis. Upregulation of CREB signaling by neural progenitor cells and neurons may promote survival and maturation of NPCs. Increased dendritic branching of mature neurons and synaptic plasticity may be mediated by presenilin-1 and APP. The factors mediating these processes are dysfunctional or compromised in Alzheimer's disease, suggesting that defective neurogenesis may affect hippocampal function in Alzheimer's disease.CC BY · PubMed Central
Figure 2 Therapeutic and translational potential of neurogenesis. Examples of current and prospective methods for the modulation and detection of neurogenesis. Means of enhancing neurogenesis include noninvasive, environmental modulations like cognitively complex activities and exercise, as well as molecular interventions like anti-depressants, pro-neurogenic small molecules, hormones or neurotransmitters, or other manipulations of the neurogenic pathways. While readouts of human neurogenesis are typically done in postmortem tissue using radioactive isotopes or analysis of neurogeneic cell markers, imaging techniques such as fMRI, or blood biomarkers will offer non-invasive avenues to determine neurogenesis during life.
Figure 2 Therapeutic and translational potential of neurogenesis. Examples of current and prospective methods for the modulation and detection of neurogenesis. Means of enhancing neurogenesis include noninvasive, environmental modulations like cognitively complex activities and exercise, as well as molecular interventions like anti-depressants, pro-neurogenic small molecules, hormones or neurotransmitters, or other manipulations of the neurogenic pathways. While readouts of human neurogenesis are typically done in postmortem tissue using radioactive isotopes or analysis of neurogeneic cell markers, imaging techniques such as fMRI, or blood biomarkers will offer non-invasive avenues to determine neurogenesis during life.CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 109 references

Research works printed but not linked: 1

  1. Lazarov, 2007, Research progress in Alzheimer's disease and dementia, 303

Cited by

Sorted by citations

See all 161

Metadata

Authors
Hollands, C., Bartolotti, N., & Lazarov, O.
Affiliations
University of Illinois Chicago (US)
Corresponding author
Lazarov, Orly
Venue
Frontiers in Neuroscience
Published
2016-05-03
Volume
10
Pages
178-178
ISSN
1662-453X (ISSN-L)
OpenAlex
W2346727851
Cited by
160
References
109
Citations by year
2026: 1 · 2025: 8 · 2024: 12 · 2023: 11 · 2022: 9 · 2021: 13 · 2020: 31 · 2019: 26 · 2018: 29 · 2017: 18 · 2016: 2
FWCI
3.11
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Neuroscience (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institute on Aging (R01AG033570, 1RC1AG036208-01 ARR)
  • U.S. Department of Defense (10917352)
  • Center for Clinical and Translational Science, University of Illinois at Chicago (CCTS-0512-06)
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
Alzheimer's disease, adult hippocampal neurogenesis, dentate gyrus, neuronal differentiation, presenilin 1, Notch1 signaling, CREB, β-catenin, hippocampal plasticity, cognitive impairment

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review