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Alzheimer Mechanisms and Therapeutic Strategies
Open accessAbstract
There are still no effective treatments to prevent, halt, or reverse Alzheimer's disease, but research advances over the past three decades could change this gloomy picture. Genetic studies demonstrate that the disease has multiple causes. Interdisciplinary approaches combining biochemistry, molecular and cell biology, and transgenic modeling have revealed some of its molecular mechanisms. Progress in chemistry, radiology, and systems biology is beginning to provide useful biomarkers, and the emergence of personalized medicine is poised to transform pharmaceutical development and clinical trials. However, investigative and drug development efforts should be diversified to fully address the multifactoriality of the disease.
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“increases its cleavage by a stress-induced neuron-specific protease [7, 12, 16]”
From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Cell-specific toxicity is the result of neuron-specific apoE4 proteolysis [7, 12].”
From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“in general, ApoE4 fragments are proposed to promote neuronal dysfunction, neurodegeneration and astrogliosis [11]”
From Apoe4 and Alzheimer’s Disease Pathogenesis—Mitochondrial Deregulation and Targeted Therapeutic Strategies (2023) · cites this paper as [11]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Nevertheless, as previously mentioned in this review, some authors identified collagenase, MMP-9, neuron-specific α-chymotrypsin-like serine protease, cathepsin D and HtrA1 as some of the proteases that are able to cleave ApoE4 into neurotoxic fragments.”
From Apoe4 and Alzheimer’s Disease Pathogenesis—Mitochondrial Deregulation and Targeted Therapeutic Strategies (2023) · cites this paper as [11]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Current targeted therapeutic strategies have failed to slow down cognitive decline in AD (Graham et al., 2017; Huang and Mucke, 2012), raising concerns about these hypotheses and calling for a broad understanding of molecular and cellular components in AD brain, at both asymptomatic and symptomatic stages during the disease progression (De Strooper and Karran, 2016).”
From Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer’s Disease Progression (2020) · cites this paper as Huang and Mucke, 2012
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In the citing paper
“Apolipoprotein E4 (APOE4) is the strongest genetic risk factor for late-onset Alzheimer’s disease (LOAD)1–3.”
From The APOE-R136S mutation protects against APOE4-driven tau pathology, neurodegeneration, and neuroinflammation (2023) · cites this paper as [1]
The cited source says what the claim attributes to it.
In the citing paper
“This is significant because astrocytes are the primary source of APOE production in the brain, and disease-related phenotypes are influenced by the interactions between astrocyte-secreted APOE and neurons (Huang, 2010; Huang and Mucke, 2012).”
From Isogenic human stem cell models reveal mutation-dependent protective mechanisms of APOE3 Christchurch (2026) · cites this paper as Huang and Mucke, 2012
The cited source says what the claim attributes to it.
In the citing paper
“lowers the age of onset [4–14]”
From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [7]
The cited source says what the claim attributes to it.
In the citing paper
“ApoE4 increases risk for AD”
From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [7]
The cited source says what the claim attributes to it.
In the citing paper
“Currently, there is no treatment to stop, prevent, or reverse AD, and recent advances with monoclonal antibody therapy targeting plaques, although controversial, might at best only slow progression (Huang and Mucke, 2012; Selkoe, 2019; Sevigny et al., 2016).”
From Inhibiting USP16 rescues stem cell aging and memory in an Alzheimer’s model (2022) · cites this paper as Huang and Mucke, 2012
In the citing paper
“The pathogenesis of the protein abnormalities, the β‐amyloid (Aβ) peptides that aggregate to form the amyloid fibrils of the neuritic plaque, and the hyperphosphorylated tau that forms the neurofibrillary tangles, is now much better understood 137 .”
From Mental health care for older adults: recent advances and new directions in clinical practice and research (2022) · cites this paper as [137]
In the citing paper
“Apolipoprotein (apo) E4, an isoform of the APOE gene in humans, is the major genetic risk factor for late-onset familial and sporadic AD [4–8], which account for most AD cases.”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [4]
In the citing paper
“Both of these pathologies are exacerbated by the presence of apoE4 [4–7, 12].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [4]
In the citing paper
“ApoE4 increases the risk and decreases the age of onset of AD in a gene dose dependent manner [4–11].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [4]
In the citing paper
“Overall, it has been demonstrated, both in vivo and in vitro, that apoE plays major roles in AD pathogenesis in both an Aβ-dependent and independent manner, and different cellular sources of apoE4 may contribute in distinct ways to AD pathogenesis [4–8, 12–14, 21, 22].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [4]
In the citing paper
“The apoE3 and apoE4 amino acid sequences differ only at position 112 where apoE4 has an Arg instead of a Cys.”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [4]
In the citing paper
“These fragments escape the secretory pathway and enter the cytosol, where they stimulate tau-phosphorylation and interact with mitochondria, leading to mitochondrial dysfunction and neurodegeneration [4].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [4]
In the citing paper
“Currently, there is no treatment to stop, prevent, or reverse AD, and recent advances with monoclonal antibody therapy targeting plaques, although controversial, might at best only slow progression (Huang and Mucke, 2012; Selkoe, 2019; Sevigny et al., 2016).”
From Inhibiting USP16 rescues stem cell aging and memory in an Alzheimer’s model (2022) · cites this paper as Huang and Mucke, 2012
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Metadata
- Authors
- Huang, Y., & Mucke, L.
- Affiliations
- Gladstone Institutes (US)
- Corresponding author
- Mucke, Lennart
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2012-03
- Volume
- 148
- Issue
- 6
- Pages
- 1204-1222
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3319071
- OpenAlex
- W2002181764
- Cited by
- 1,758
- References
- 211
- Citations by year
- 2026: 37 · 2025: 80 · 2024: 78 · 2023: 104 · 2022: 113 · 2021: 127 · 2020: 148 · 2019: 149 · 2018: 160 · 2017: 149 · 2016: 168 · 2015: 143 · 2014: 135 · 2013: 127 · 2012: 39
- FWCI
- 15.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (AG011385, AG022074, P01AG022074)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, disease mechanisms, treatment options, genetic risk factors, transgenic animal models, biomarkers, personalized medicine, drug development, complex diseases
- MeSH terms
- Alzheimer Disease, Animals, Cognition, gamma-Aminobutyric Acid, Humans, Amyloid beta-Protein Precursor
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