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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Alzheimer's disease (AD) involves a dynamic interaction between neuroinflammation and metabolic dysregulation, where microglia play a central role.
Why it matters
This review describes how microglia change their metabolism in Alzheimer's disease, with genes such as TREM2, APOE and HIF-1α involved. It reports no treatment, cure or prevention; it only outlines a research direction.
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This narrative review examines the utility of gait digital biomarkers in Parkinson's disease (PD) research and clinical trials across four contexts: disease susceptibility/risk, disease progression, response to exercise, and fall prediction.
Why it matters
This review is about digital gait biomarkers in Parkinson's disease for tracking risk, progression, exercise response, and falls. It provides no information relevant to treating, curing, or preventing Alzheimer's disease.
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= 0.029). Despite the absence of overt nOH, patients with DLB show covert dysautonomia encompassing adrenergic, parasympathetic, and sudomotor dysfunction, highlighting the importance of standardized autonomic evaluation.
Why it matters
This cohort study found that patients with dementia with Lewy bodies show covert dysautonomia affecting adrenergic, parasympathetic and sudomotor function even without overt orthostatic hypotension, and that those with normal DaT-SPECT had greater peripheral autonomic impairment. The authors call for further research into autonomic dysfunction across dementia with Lewy bodies subtypes and stages, and no treatment, cure or prevention is reported.
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Model scores two standard deviations below the mean had 4 months increased survival (two standard deviations below had 3 months decreased survival).
Why it matters
An AI model using F-wave responses estimated the likelihood of ALS and survival risk, with model scores two standard deviations below the mean linked to 4 months increased survival and two standard deviations above linked to 3 months decreased survival. This concerns ALS, not Alzheimer's disease, and offers no treatment, cure, or prevention for dementia.
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50/100
Of 11 subjects with average AUCs above 500,000 units, 7 (64%) developed a central LBD compared to 1 of 20 (5%), with AUCs below the cutoff value (P = 0.0011 by log-rank test).
Why it matters
This longitudinal study found that elevated cerebrospinal fluid alpha-synuclein seeding activity predicts central Lewy body diseases, with 64% of those above a cutoff developing LBD compared to 5% below. It supports a predictive biomarker but does not provide a treatment or cure.
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The association between dysfunctional microglia and amyloid-β (Aβ) is a fundamental pathological event and increases the speed of Alzheimer's disease (AD).
Why it matters
This study describes a nanovesicle system that delivers BACE1 siRNA and a TREM2 plasmid to modulate microglia and amyloid-beta in a gene therapy approach. It is a laboratory-based strategy, so it does not yet show any treatment, cure or prevention for Alzheimer's disease in people.
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Adult individuals with Down syndrome (DS) develop Alzheimer disease (AD).
Why it matters
Using cryo-electron microscopy on two Down syndrome brains, this study found two amyloid beta 40 filament types that differ from sporadic Alzheimer disease and amyloid beta 42 and tau filaments identical to those in Alzheimer disease. It describes protein structure only and does not test any treatment, though the authors note it may help assess whether adults with Down syndrome could join Alzheimer clinical trials.
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& aims Hepatic stellate cells (HSCs) are the key drivers of fibrosis in metabolic dysfunction-associated steatohepatitis (MASH), the fastest growing cause of hepatocellular carcinoma (HCC) worldwide.
Why it matters
This study characterizes senescent hepatic stellate cells in metabolic dysfunction-associated steatohepatitis, a liver disease, in human and mouse tissue. It is about liver disease and not Alzheimer's disease, so it has no implications for treating, curing or preventing Alzheimer's.
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Cancer mortality primarily stems from metastatic recurrence, emphasizing the urgent need for developing effective metastasis-targeted immunotherapies.
Why it matters
This study is about breast cancer lung metastases and identified TREM2 macrophages at the metastatic boundary in mice. It provides no evidence about treating, curing, or preventing Alzheimer's disease.
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Microglia-mediated neuroinflammation plays a crucial role in the pathogenesis of Parkinson's disease (PD).
Why it matters
In mice and cells modeling Parkinson's disease, loss of TREM2 worsened activation of the NLRP3 inflammasome and a form of cell death called pyroptosis. This is animal and cell research on Parkinson's disease and does not directly inform Alzheimer's treatment, cure or prevention.
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Atherosclerosis is driven by the expansion of cholesterol-loaded 'foamy' macrophages in the arterial intima.
Why it matters
This study is about atherosclerosis and shows that Trem2 is associated with foamy macrophage specification, with loss of Trem2 reducing the ability of foamy macrophages to take up oxidized low-density lipoprotein. It concerns plaque macrophages in arteries, not Alzheimer's disease, and provides no direct information about treating, curing or preventing Alzheimer's.
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Primary sclerosing cholangitis (PSC) is an immune-mediated cholestatic liver disease for which pharmacological treatment options are currently unavailable.
Why it matters
This study is about primary sclerosing cholangitis, a liver disease, not Alzheimer's disease. It has no direct meaning for Alzheimer's treatment or prevention.
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Herbal medicines demonstrate great potential to prevent cognitive impairment.
Why it matters
This review gathered experimental studies on herbal medicines, such as Ginkgo biloba and ginseng, that act on the neurovascular glial unit, the team of blood vessel, support and nerve cells that keeps the brain healthy. Active components showed potential to improve blood-brain barrier function and blood flow and to calm inflammatory glial cells. The authors see great potential for preventing cognitive impairment, but the evidence comes from experimental studies rather than proven benefits in patients.
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Lysosome dysfunction arises early and propels Alzheimer's disease (AD).
Why it matters
This study shows that the phosphorylated 682 YENPTY motif of APP-betaCTF binds the v-ATPase V0a1 subunit and competitively inhibits v-ATPase, disrupting lysosome function in Down syndrome fibroblasts and mouse brains. Lowering this phosphorylation restored v-ATPase and lysosome function in cells and in mice, but these are laboratory and animal findings, not a tested treatment for people.
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& aims The immune landscape of hepatocellular carcinoma (HCC) following transarterial chemoembolisation (TACE) remains to be clarified.
Why it matters
This study is about liver cancer treated with transarterial chemoembolisation, not Alzheimer's disease, so it provides no direct information about treating, curing or preventing Alzheimer's. Its findings on TREM2-positive macrophages and CD8-positive T cells come from human liver tumour samples and mouse models of liver cancer.
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The TREM2-DAP12 receptor complex sustains microglia functions.
Why it matters
Single-nucleus RNA-sequencing of brain specimens from people with DAP12-deficient Nasu-Hakola disease revealed a unique microglia signature. It describes a rare early-onset dementia and does not test a treatment or cure for Alzheimer's disease.
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This study has established a panel of highly important DEGs to signify the potential therapeutic targets for neuroregenerative strategy against pathogenic events associated with cerebral stroke.
Why it matters
Combining gene activity data from 97 samples of rat brains after an experimental stroke, researchers found 939 genes that were altered, 30 of them tied to neural stem cells and new nerve cell growth, with some overlap in human stroke brain tissue. The authors propose these genes as possible targets for helping the brain repair itself after stroke. This is mainly animal data on stroke, so any relevance to dementia treatment remains a hypothesis.
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50/100
Brain Aβ deposition is a key early event in the pathogenesis of Alzheimer´s disease (AD), but the long presymptomatic phase and poor correlation between Aβ deposition and clinical symptoms remain puzzling.
Why it matters
In mice, blocking Aβ production reduced Aβ deposits but did not stop the rise of a neurodegeneration marker, suggesting Aβ buildup and nerve damage are not tightly linked. This is animal research, so it does not yet show whether the same is true in people or whether any treatment approach would work.
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Forty-six clinically normal older adults (mean age = 70 years; 43% female) were included.
Why it matters
In 46 clinically normal older adults, higher CSF synaptic proteins moderated the link between axonal injury marker NfL and later temporoparietal atrophy. This is a small longitudinal biomarker study and does not test any treatment, cure or prevention.
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TYROBP (also known as DAP12 or KARAP) is a transmembrane adaptor protein initially described as a receptor-activating subunit component of natural killer (NK) cells.
Why it matters
This review describes TYROBP/DAP12 as the downstream adaptor and putative signaling partner for several microglial receptors implicated in Alzheimer's disease, including TREM2. It is a discussion of signaling biology and reports no treatment, cure or prevention.
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CSF NfL is a non-specific marker of aging and white matter integrity with limited sensitivity to specific markers of AD.
Why it matters
In 419 participants, cerebrospinal fluid neurofilament light chain increased with age and was more strongly related to white matter hyperintensity volume and age than to Alzheimer marker status. This concerns a marker of aging and white matter damage, not a treatment, cure or prevention of Alzheimer's disease.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane receptor of the immunoglobulin superfamily that is secreted in a soluble (sTREM2) form.
Why it matters
This laboratory study found that soluble TREM2 inhibits secondary nucleation of amyloid beta fibrillization and enhances cellular uptake of fibrillar amyloid beta. These are in-vitro findings about amyloid beta behavior and do not yet show a treatment, cure or prevention for Alzheimer's disease.
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The alteration of the insulin-signaling/mTOR pathways represents an early event in DS brain and likely contributes to the cerebral dysfunction and intellectual disability observed in this unique population.
Why it matters
This study found signs of insulin resistance and activation of the mTOR pathway in neuronal-derived extracellular vesicles from children with Down syndrome. It suggests these changes occur early in the brain, but it does not test any treatment or prevention for Alzheimer disease.
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50/100
Late-onset Alzheimer's disease (AD; LOAD) is the most common human neurodegenerative disease, however, the availability and efficacy of disease-modifying interventions is severely lacking.
Why it matters
This paper describes a new mouse model expressing humanized APOEε4 and Trem2*R47H to better model late-onset Alzheimer's disease. It is animal model development, so it is early and does not yet show a treatment for people.
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Human genetic association studies point to immune response and lipid metabolism, in addition to amyloid-beta (Aβ) and tau, as major pathways in Alzheimer's disease (AD) etiology.
Why it matters
In mice, adult-onset loss of brain sulfatide was sufficient to cause Alzheimer's-like neuroinflammation and cognitive impairment. This is animal evidence about a possible disease mechanism and does not show a treatment, cure, or prevention for people.
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.
- TREM2 in CNS homeostasis and neurodegenerative disease
- Effects of Heparan Sulfate Trisaccharide Containing Oleanolic Acid in Attenuating Hyperphosphorylated Tau-Induced Cell Dysfunction Associated with Alzheimer’s Disease
- Association of Retinal Nerve Fiber Layer Thinning With Current and Future Cognitive Decline: A Study Using Optical Coherence Tomography
- Beyond Dizziness: Virtual Navigation, Spatial Anxiety and Hippocampal Volume in Bilateral Vestibulopathy
- BIOMARCADORES BIOQUÍMICOS EMERGENTES PARA EL DIAGNÓSTICO TEMPRANO DE ENFERMEDADES NEURODEGENERATIVAS: REVISIÓN SISTEMÁTICA
- A Drosophila model for TDP-43 proteinopathy
- Effects of α‐synuclein pathology on synaptic dysfunction and clinical outcomes in normal aging
- [Transgenic mice overexpressing copper-zinc superoxide dismutase: a model for the study of radical mechanisms and aging]
- Parkinson disease neuropathology: later-developing dementia and loss of the levodopa response
- Anti-human TREM2 induces microglia proliferation and reduces pathology in an Alzheimer's disease model