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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Microglia-mediated neuroinflammation is widely associated with seizures and epilepsy.
Why it matters
This study examines complement molecules and microglia in human epilepsy, not Alzheimer's disease. It reports altered mRNA levels of complement molecules in epilepsy but provides no information on treating, curing or preventing Alzheimer's disease.
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Lewy body disorders (LBD) are common neurodegenerative diseases characterized by the presence of aggregated α-synuclein in Lewy bodies and Lewy neurites in the central and peripheral nervous systems.
Why it matters
In 63 cases of Lewy body disorders, most brains had two or three coexisting pathologies, and amyloid score was the best correlate of time to dementia in Parkinson disease. This is an autopsy mapping study and does not test any treatment or prevention.
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44/100
The percentage of unmetabolized 18 F-T807 in plasma followed a single exponential with a half-life of 17.0 ± 4.2 min. Metabolite-corrected plasma radioactivity concentration fit a biexponential (half-lives, 18.1 ± 5.8 and 2.4 ± 0.5 min). 18 F-T807 in gray matter peaked quickly (SUV > 2 at ∼5 min).
Why it matters
This pharmacokinetic study found that the tau PET radiotracer 18F-T807 showed rapid clearance from plasma and properties suitable for quantifying tau with PET, and that simplified imaging approaches correlated well with more complex methods. It is a technical imaging study, not a test of treating, curing, or preventing Alzheimer's disease.
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44/100
Rare variation in TREM2 has been associated with greater risk for Alzheimer's disease (AD).
Why it matters
Across two independent Alzheimer's disease cohorts, a gene-level test (SKAT) found rare TREM2 variants, not previously studied at the protein level, to be enriched in people with AD. When tested in cells, two newly described variants, S31F and R47C, put noticeably less TREM2 on the cell surface. This links more rare TREM2 changes to a possible loss of the receptor on microglia, but it is genetic and lab-based evidence: it does not give personal risk figures or show that raising TREM2 would treat or prevent Alzheimer's disease.
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Our current studies indicate that thrombin and HMGB1 are causal proximate proinflammatory mediators of BBB dysfunction, while sTM levels may indicate BBB endothelial damage; HMGB1 and sRAGE might serve as clinical biomarkers for progression and/or therapeutic efficacy along the AD spectrum.
Why it matters
This study found higher blood levels of HMGB1 and sRAGE in people with Alzheimer's disease that tracked with amyloid beta levels, and it examined how these molecules affect the blood-brain barrier in cells in the laboratory. These are proposed biomarkers of inflammation and barrier damage, not a treatment, and the work is early and laboratory-based.
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Sphingosine-1-phosphate (S1P) and S1P receptors (S1PR) are ubiquitously expressed.
Why it matters
This review covers sphingosine-1-phosphate signaling and its role in immune trafficking, noting that the drug FTY720 reduces relapses in multiple sclerosis. It focuses on autoimmunity and inflammation generally, not Alzheimer's disease, so it offers no direct treatment, cure or prevention for Alzheimer's.
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The importance of TANK binding kinase-1 (TBK1), a multimeric kinase that modulates inflammation and autophagy, in human health has been highlighted for the first time by the recent discoveries of mutations in TBK1 that underlie amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), normal tension glaucoma (NTG) or childhood herpes simplex encephalitis (HSE).
Why it matters
This review discusses TBK1 mutations linked to ALS, frontotemporal dementia, normal tension glaucoma and childhood herpes simplex encephalitis, and TBK1's role in neuroinflammation. It concerns these other conditions and does not report a treatment, cure or prevention for Alzheimer's disease.
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Vascular dementia (VD) is defined as a progressive neurodegenerative disease of cognitive decline, attributable to cerebrovascular factors.
Why it matters
This review of animal models describes chronic cerebral hypoperfusion as associated with the initiation and progression of vascular dementia and Alzheimer's disease. It reports no treatment, cure, or prevention for people.
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Traumatic brain injury (TBI) affects 1.7 million persons annually in the United States (Centers for Disease Control and Prevention).
Why it matters
In mice with traumatic brain injury, lacking TREM2 changed macrophage distribution and improved recovery. This is early animal work on brain injury, and it does not show that any treatment prevents or cures Alzheimer's disease in people.
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Recent genome-wide association studies revealed TREM2 rs75932628-T variant to be associated with Alzheimer's disease (AD) and other neurodegenerative diseases.
Why it matters
This study measured TREM2 mRNA levels and DNA methylation in human hippocampus from neuropathologically confirmed controls and pure Alzheimer's disease cases. It is an observational analysis of brain tissue and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Toll-like receptors (TLR) are transmembrane pattern recognition receptors that recognize microbial ligands and signal for production of inflammatory cytokines and type I interferon in macrophages and dendritic cells (DC).
Why it matters
This review describes how the body dampens Toll-like receptor signaling to avoid excessive inflammation, using examples from autoimmune diseases such as rheumatoid arthritis and lupus. It is about immune regulation in general and does not report any Alzheimer's treatment, cure or prevention findings.
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Alzheimer disease (AD) is characterized by the extracellular accumulation of amyloid β (Aβ), which is accompanied by a robust inflammatory response in the brain.
Why it matters
In a mouse model of Alzheimer disease, combining two drugs that target LXR and PPARγ reduced amyloid beta levels and improved behavior. These are early animal findings, and it is not yet known whether the same combination would be safe or effective in people.
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44/100
Traumatic brain injury (TBI) has been linked to dementia and chronic neurodegeneration.
Why it matters
This review discusses links between traumatic brain or spinal cord injury, sustained neuroinflammation and progressive neurodegeneration, including chronic traumatic encephalopathy. It does not report a treatment or cure for Alzheimer's disease.
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Our results indicate that SHR share behavioral and neuropathological characteristics with human cSVD patients and further undergird the relevance of immune responses for the initiation and progression of cSVD.
Why it matters
This animal study found that middle-aged hypertensive rats exhibited non-spatial memory deficits, brain atrophy, white matter demyelination, and neuroinflammation compared to normotensive rats. It suggests that these rats share behavioral and neuropathological characteristics with human cerebral small vessel disease, but the findings are from an animal model.
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Neuroinflammatory changes play a pivotal role in the progression of Parkinson's disease (PD) pathogenesis.
Why it matters
This mouse study of a Parkinson's disease model discusses microglial polarization and its possible link to Alzheimer's disease progression, suggesting modulation of microglia as a possible neuroprotective target. It is an animal study and provides no treatment, cure or prevention for Alzheimer's disease.
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The mammalian target of rapamycin (mTOR) signaling pathway is a key developmental pathway involved in mechanisms underlying cellular aging and neurodegeneration.
Why it matters
In developing hippocampi from people with Down syndrome, components of the mTOR signaling pathway were increased compared with controls and persisted after birth. This is a post-mortem tissue study suggesting dysregulated mTOR may contribute to early developmental abnormalities, not a treatment trial.
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44/100
Our results suggest that IF induces adaptive responses in the brain and periphery that can suppress inflammation and preserve cognitive function in an animal model of systemic bacterial infection.
Why it matters
In this rat study, intermittent fasting reduced memory impairment and neuroinflammation caused by lipopolysaccharide. It is an animal study and does not show that intermittent fasting prevents or treats Alzheimer's disease in people.
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Recently, 3 rare coding variants significantly associated with Alzheimer's disease (AD) risk have been identified in western populations using whole exome sequencing method, including p.R47H in TREM2, p.V232M in PLD3, and p.T835M in UNC5C. To examine whether these variants are genetic risk factors in patients with AD from mainland China, we sequenced exon 2 of TREM2, exon 9 of PLD3, and exon 15 of UNC5C in Chinese Han population including 360 patients with AD and 400 control individuals.
Why it matters
Three rare gene changes tied to higher Alzheimer's risk in Western studies (TREM2 R47H, PLD3 V232M, UNC5C T835M) did not turn up in a single person among 360 Han Chinese patients and 400 controls from mainland China, so the authors conclude they "might not play an important role in AD risk in mainland China." The researchers did find five previously unreported changes, one in TREM2 and four in UNC5C, in late-onset patients, but the study does not show that these raise risk. It describes genetics only, not treatment or prevention.
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Phosphorylation of tau protein at the carboxyl terminus may be among the earliest tau events, and it occurs prior to the apparition of the classical fibrillar structure.
Why it matters
This study found that a specific chemical modification of the tau protein appears early in the formation of tangles in Alzheimer's disease and Down syndrome brains. It describes a step in the disease process but does not test or propose a treatment or cure.
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TREM2 has been reported to be associated with Alzheimer's disease (AD).
Why it matters
People with Alzheimer's disease had higher levels of TREM2 mRNA and protein in their blood than healthy controls, and these levels correlated with cognitive test scores. The diagnostic accuracy of TREM2 protein on monocytes was 70%, which is not high enough on its own to serve as a stand-alone diagnostic test.
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Alzheimer disease (AD) results, in part, from the excess accumulation of the amyloid-β (Aβ) peptide as neuritic plaques in the brain.
Why it matters
The microRNA miR-339-5p was found to lower BACE1 protein levels in human brain cell cultures, and its levels were reduced in brain tissue from Alzheimer's disease subjects. This identifies a possible regulatory pathway and drug target, but no treatment based on it has been tested in patients.
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Perturbation of lipid metabolism favours progression of Alzheimer disease, in which processing of Amyloid Precursor Protein (APP) has important implications.
Why it matters
This laboratory work found that the amyloid precursor protein helps control cholesterol production in neurons, linking APP processing and lipid metabolism. It was done in cells, so it does not yet show how this could be used to treat or prevent Alzheimer's disease in people.
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γ-Secretase is an intramembrane aspartyl protease that cleaves the amyloid precursor protein to produce neurotoxic β-amyloid peptides (i.e. Aβ42) that have been implicated in the pathogenesis of Alzheimer disease.
Why it matters
This laboratory study used photoaffinity probes to show that different classes of gamma-secretase modulators bind to distinct allosteric sites on presenilin. It clarifies how these compounds work but does not show that they treat, cure, or prevent Alzheimer's disease in people.
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The Northwestern University SuperAging Project recruits community dwellers over the age of 80 who have unusually high performance on tests of episodic memory.
Why it matters
This preliminary study of people over 80 with unusually high memory performance found some had higher cortical thickness, low levels of age-related Alzheimer pathology, and a lower frequency of the apolipoprotein E ɛ4 allele. It is early observational work offering clues about possible factors promoting resistance to age-related brain changes, not a treatment, cure, or prevention.
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Current evidence suggests a central role for autophagy in Alzheimer disease (AD), and dysfunction in the autophagic system may lead to amyloid-β (Aβ) accumulation.
Why it matters
In in vitro and in vivo Alzheimer's disease models, mesenchymal stem cells enhanced autophagy and increased amyloid-beta clearance. This is early model-based work and does not establish any treatment, cure or prevention for people with 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.
- Endothelial nitric oxide modulates expression and processing of amyloid precursor protein
- Hypersensitivity to ionizing radiation in cultured cells from Down syndrome patients
- Loss of C9ORF72 impairs autophagy and synergizes with polyQ Ataxin-2 to induce motor neuron dysfunction and cell death
- Developmental regulation of TREM2 and DAP12 expression in the murine CNS: implications for Nasu-Hakola disease
- Comparative mapping of DNA markers from the familial Alzheimer disease and Down syndrome regions of human chromosome 21 to mouse chromosomes 16 and 17
- Association of Favorable Cerebrospinal Fluid Markers With Reversion of Mild Cognitive Impairment Due to Parkinson’s Disease
- DNA repair factor BRCA1 depletion occurs in Alzheimer brains and impairs cognitive function in mice
- Senile myoclonic epilepsy in Down syndrome: a video and EEG presentation of two cases
- Endogenous amyloid-β is necessary for hippocampal synaptic plasticity and memory
- TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration