Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Chronic cerebral hypoperfusion (CCH) is regarded as a high-risk factor for cognitive decline in vascular dementia (VaD).
Why it matters
In rats with chronic cerebral hypoperfusion plus diabetes, curcumin protected against cognitive impairment by suppressing neuroinflammation, apoptosis and pyroptosis. This is animal research only and reports no treatment, cure or prevention for people.
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Dysregulation of brain insulin signaling with reduced downstream neuronal survival and plasticity mechanisms are fundamental abnormalities observed in Alzheimer disease (AD).
Why it matters
In a mouse model of Down syndrome, brain insulin signaling and related energy, oxidative stress, and synaptic pathways were impaired starting early in life. These are animal findings and do not test any treatment in people.
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Chronic dialysis is associated with relatively high mortality and increased comorbidities that may render the patient unsuitable for renal transplantation.
Why it matters
This paper suggests patient selection criteria for initial clinical trials of pig kidney xenotransplantation in the United States. It notes that life-supporting genetically modified pig kidney transplantation in nonhuman primates is currently associated with substantial success, with recipient survival extending for many months or more than a year.
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Periodontitis is the sixth most prevalent diseases around the globe, which is closely related to many systemic diseases and affects general health.
Why it matters
This study is about periodontitis and found Trem2 regulates osteoclast formation through Syk-dependent ROS signaling. It has no bearing on treating, curing, or preventing Alzheimer's disease.
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TREM2 is a microglial cell surface receptor, with risk mutations linked to Alzheimer's disease (AD), including R47H. TREM2 signalling via SYK aids phagocytosis, chemotaxis, survival, and changes to microglial activation state.
Why it matters
In this human iPSC-derived macrophage model, the TREM2 R47H variant caused transcriptional dysregulation similar to TREM2 knockout but only subtle functional phenotypes. This is a cell-based laboratory study, so it does not show whether these changes affect Alzheimer's disease in people.
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Neuropathic pain (NeuP) is a chronic and challenging clinical problem, with little effective treatment.
Why it matters
This rat study explored whether resveratrol ameliorates neuroinflammation and produces anti-mechanical allodynia effects via regulating TREM2 in spared nerve injury. It concerns neuropathic pain in rats and does not report any treatment, cure, or prevention for Alzheimer's disease.
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Air pollution has become one of the most serious issues for human health and has been shown to be particularly concerning for neural and cognitive health.
Why it matters
In BV-2 microglial cells, astaxanthin suppressed PM2.5-induced neuroinflammation by regulating Akt phosphorylation. This is a cell-based laboratory study and does not yet show a treatment, cure, or prevention for Alzheimer's disease in people.
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Vascular dementia is the second-most cause of dementia, characterized by cerebral infarcts, white matter lesions, myelin loss and often amyloid angiopathy.
Why it matters
This paper states that abnormal neuroinflammation, autophagy and apoptosis are prerequisite factors for endothelial and neuronal cell damage in vascular dementia. It is a review of mechanisms in vascular dementia and reports no treatment or cure.
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Obesity is a multifactorial disease in which environmental conditions and several genes play an important role in the development of this disease.
Why it matters
This review describes shared biological mechanisms like insulin resistance and inflammation between obesity and Alzheimer's, and notes that several genes in the leptin-melanocortin pathway are linked to both conditions. It suggests that environmental and genetic factors common to obesity may also influence neurodegenerative disease, but no treatment or prevention is tested.
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Down syndrome (DS) is the most common genetic cause of intellectual disability that is associated with an increased risk to develop early-onset Alzheimer-like dementia (AD).
Why it matters
This review discusses how the BACH1/Nrf2 axis may regulate oxidative stress in Down syndrome and its transition to Alzheimer-like dementia. It states that the role of this axis is still under investigation and that effects of triplicated BACH1 on Nrf2 regulation are unknown, so it does not provide a treatment or cure.
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Alzheimer disease (AD) is a complex neurodegenerative disorder with no definite treatment.
Why it matters
This rat study tested exosomes containing miR-29b as a possible way to deliver treatment, since miR-29 family expression is reduced in Alzheimer's disease. It is animal research and does not establish a treatment or cure for people.
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43/100
Triggering receptor expressed on myeloid cells 2 (TREM2) serves as an anti-inflammatory receptor, negatively regulating the innate immune response.
Why it matters
In pig cells, TREM2 acted as an anti-inflammatory receptor and its presence helped a virus called PRRSV replicate, while silencing TREM2 restrained the virus. This is infectious disease research in animals and does not directly inform Alzheimer's treatment, cure or prevention.
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Depression is a severe neuropsychiatric disorder, of which the underlying pathological mechanisms remain unclear.
Why it matters
In rodent models, a ketogenic diet reduced depressive-like behaviors and was linked to restored microglial activation and neuronal excitability in the lateral habenula. This is animal work about depression and does not report any treatment, cure, or prevention for Alzheimer's disease.
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Adipose tissue remodeling plays a significant role in obesity-induced insulin resistance.
Why it matters
In mice fed a high-fat diet, the study investigated whether TREM2 regulates obesity-induced insulin resistance through adipose tissue remodeling. It is about obesity and insulin resistance in mice, not Alzheimer's disease, so it has no implications for treating, curing or preventing Alzheimer's.
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Neurofilament light chain (NFL) has been recently introduced as a biomarker of early dementia. 18-Fluorodeoxyglucose positron emission tomography (18F-FDG-PET) is a proxy for regional hypometabolism in Alzheimer disease (AD).
Why it matters
Among 149 patients with mild cognitive impairment, higher baseline plasma neurofilament light chain levels correlated with hypometabolism in Alzheimer's signature brain regions. This is a biomarker-imaging correlation study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Variants in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) are known to increase the risk of developing Alzheimer disease and Parkinson's disease (PD).
Why it matters
In cell and mouse models of Parkinson's disease, loss of TREM2 function worsened alpha-synuclein-induced neurodegeneration and neuroinflammation. This study is about Parkinson's disease models and does not show any treatment, cure, or prevention for Alzheimer's disease.
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Microglia have important remodeling functions in neurodevelopment, aging, and disease, with evidence for molecular diversity.
Why it matters
This study profiled microglia in the developing murine retina and found a population resembling aging and disease-associated microglia, with TREM2 signalling modulating select genes. It is mouse developmental research and does not report any treatment, cure, or prevention for Alzheimer's disease.
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Flaviviruses account for most arthropod-borne cases of human encephalitis in the world.
Why it matters
In mice with flavivirus brain infection, using a drug to deplete microglia increased viral load in the brain and raised mortality. This shows microglia help control this viral infection, but it concerns infectious disease in animals and not Alzheimer's treatment, cure or prevention.
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The gram-negative facultative anaerobe Bacteroides fragilis (B. fragilis) constitutes an appreciable proportion of the human gastrointestinal (GI)-tract microbiome.
Why it matters
This paper describes how a neurotoxin from a gut bacterium, Bacteroides fragilis, may promote inflammatory neurodegeneration and has been found in Alzheimer's disease brain tissue. It is a mechanistic and observational report, not a trial, so it does not show that targeting this bacterium treats or prevents the disease.
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Several parameters representing the clinical diversity of Parkinson's disease (PD), including severity, phenotypes, cognitive decline, anxiety and depression were analyzed to examine the link with interleukin-1β (IL-1β), the interleukin-1 receptor antagonist (IL-1RA), IL-6, IL-10, and tumor necrosis factor-α (TNFα) and also to determine the relationship between levels of these factors in serum and cerebrospinal fluid (CSF).
Why it matters
In Parkinson's disease, elevated serum IL-1β and IL-6 and reduced IL-1RA were found, and increased cerebrospinal fluid TNFα indicated rapid progression. Lower serum TNFα was seen in Parkinson's patients with mild cognitive impairment compared with controls, but this study concerns Parkinson's disease, not Alzheimer's disease treatment or prevention.
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Triggering receptor expressed on myeloid cells-2 (TREM2) was a newly identified receptor expressed on microglia.
Why it matters
In mice whose dopamine-producing neurons were damaged with the toxin MPTP (a lab model of Parkinson's disease), the authors report that raising TREM2 levels "remarkably reduced" the nerve-cell loss and brain inflammation. They trace the effect to TREM2 dampening the TLR4/TRAF6 route to MAPK and NF-κB inflammatory signalling. This is an animal study in a different disease, so it does not show any treatment or prevention for Alzheimer's disease in people.
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The increase of pro-inflammatory cytokines is associated with dementia, Parkinson's disease, atherosclerosis, diabetes type 2, sarcopenia and a high risk of morbidity and mortality.
Why it matters
This review describes immunosenescence as a state of chronic inflammation with up-regulation of pro-inflammatory cytokines, and states that the increase of pro-inflammatory cytokines is associated with dementia and Parkinson's disease. It discusses aging and immune changes but does not test any treatment or prevention for Alzheimer's disease.
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The findings of this study are consistent with previous reports demonstrating a high aggregation propensity of Aβ 4-x peptides and suggest an important role of these N-truncated Aβ species in the process of amyloidogenesis and plaque core formation.
Why it matters
This study made new antibodies and found a truncated form of amyloid-beta mainly in plaque cores and blood vessel amyloid in Alzheimer disease, Down syndrome, and mouse models. It is laboratory work and does not test treatment, cure, or prevention.
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The amyloid precursor protein (APP) is a type I transmembrane glycoprotein better known for its participation in the physiopathology of Alzheimer disease as the source of the beta amyloid fragment.
Why it matters
This review focuses on the normal physiological role of amyloid precursor protein as a cell adhesion molecule in neuronal development, including migration, neurite outgrowth, and synaptogenesis. It discusses how APP overexpression in Down syndrome might contribute to neuronal and synaptic defects, but it reports no treatment, cure, or prevention.
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Amyotrophic lateral sclerosis (ALS) is a fatal adult-onset neurodegenerative disorder affecting motor neurons (MNs).
Why it matters
This study concerns amyotrophic lateral sclerosis, showing that exosomes from cells with mutant SOD1 are enriched in miR-124 and alter microglia phenotype. It does not address treating, curing or preventing Alzheimer's disease.
From across this topic
10 of the 4,748 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Distinctive pattern of Bergmann glial pathology in human hepatic encephalopathy
- Synaptic markers of cognitive decline in neurodegenerative diseases: a proteomic approach
- Twenty years of therapeutic development in tauopathy mouse models: a scoping review
- Cholesterol accumulates in senile plaques of Alzheimer disease patients and in transgenic APP(SW) mice
- Symmetric diffeomorphic image registration with cross-correlation: evaluating automated labeling of elderly and neurodegenerative brain
- A rare coding variant in TREM2 increases risk for Alzheimer's disease in Han Chinese
- Oxysterols as biomarkers in neurodegenerative diseases
- TDP-43 Proteinopathy and ALS: Insights into Disease Mechanisms and Therapeutic Targets
- Molecular imaging of microglial activation in amyotrophic lateral sclerosis
- Small vessel disease: mechanisms and clinical implications