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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The patient was participating in an extended open-label trial of aducanumab when she was admitted to hospital for focal seizures and ARIA in 2 noncontiguous regions of the left frontal and occipital lobes.
Why it matters
This case report describes a 75-year-old patient with mild cognitive impairment due to Alzheimer's disease who developed fatal super-refractory status epilepticus related to severe amyloid-related imaging abnormalities while in an extended open-label aducanumab trial. It reports a serious harm in a single patient, not a treatment, cure or prevention benefit.
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The accessibility of the retina with the use of non-invasive and relatively low-cost ophthalmic imaging techniques and analytics provides a unique opportunity to improve the detection, diagnosis and monitoring of systemic diseases.
Why it matters
This Roadmap from a National Heart, Lung, and Blood Institute workshop describes current knowledge gaps and research opportunities to evaluate relationships between retinal biomarkers and risk of cardiovascular diseases, including vascular dementia. Identified gaps include the need to simplify and standardize image capture by non-ophthalmic health workers and to conduct longitudinal studies using multidisciplinary networks of diverse at-risk populations.
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This meta-analysis revealed a significant reduction in sRAGE in neurocognitive and neuropsychiatric disorders particularly in Asians and moderate age.
Why it matters
Pooling 16 studies, this meta-analysis found that people with neurocognitive disorders (n = 1444) and neuropsychiatric disorders (n = 444) had lower blood levels of sRAGE than healthy controls. sRAGE acts as a decoy that soaks up advanced glycation end products, which can drive inflammation, and dementia patients were among those with lower levels. These are associations across studies, so they suggest sRAGE could be a biomarker rather than showing it causes disease.
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Mental symptoms have been shown to be associated with dementia.
Why it matters
This longitudinal study investigated whether anxiety increases the risk of cognitive decline in older adults without dementia and explored possible biological processes. It does not test a treatment for anxiety or dementia, and the findings are observational.
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Despite advances in uncovering the mechanisms that underlie neuroinflammation and neurodegenerative disease, therapies that prevent neuronal loss remain elusive.
Why it matters
This review argues that because targeting amyloid-β and tau has "been met with limited success," these proteins likely act within a wider disease network, one that "could involve" astrocytes, brain support cells that "adopt reactive states" under stress. It reports that gene-activity studies in patients and disease models point to "many putative reactive sub-states" of astrocytes, and that how far these are shared across diseases "is unclear." It is a review with no new data and reports no treatment, cure or prevention.
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56/100
The presence of multiple additive pathologies associated with older age, increasing disease duration, APOE e4 allele and presence of dementia across the clinical groups.
Why it matters
This work reports that neurodegenerative disease often involves multiple additive pathologies, associated with older age, longer disease duration, the APOE e4 allele, and dementia. This heterogeneity means the total pathological burden is often more than a single expected clinicopathological correlation, which matters for how disease is classified and studied.
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Non-alcoholic fatty liver disease (NAFLD) is a common, progressive liver disease strongly associated with the metabolic syndrome.
Why it matters
This study provides a proteo-transcriptomic map of steatohepatitis and fibrosis in non-alcoholic fatty liver disease, characterizing circulating proteins in 306 patients. It concerns liver disease, not Alzheimer's disease, and reports no Alzheimer's treatment, cure or prevention.
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We selected the cerebellum as a pseudo-reference region based on the immunohistochemical comparison of age-matched PS2APP and WT mice.
Why it matters
In a mouse model of Alzheimer's disease, a PET tracer for reactive astrogliosis showed increased signal in the hippocampus and thalamus before changes in TSPO and amyloid PET, and first-in-human scans matched expected patterns in neurodegenerative conditions. This is early preclinical and first-in-human work, so it does not yet show a benefit for diagnosing or treating Alzheimer's disease in patients.
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Although the discovery of the critical role of α-synuclein (α-syn) in the pathogenesis of Parkinson's disease (PD) is now twenty-five years old, it still represents a milestone in PD research.
Why it matters
This review discusses how abnormal forms of alpha-synuclein cause neuronal death and early synaptic changes in Parkinson's disease and related disorders such as dementia with Lewy bodies. It states that understanding these early mechanisms is important for research on biomarkers and possible disease-modifying therapies targeting alpha-synuclein, but reports no treatment, cure, or prevention.
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Reliable noninvasive biomarkers are an unmet clinical need for the diagnosis of NASH.
Why it matters
This study examined plasma TREM2 as a diagnostic biomarker for NASH in patients with elevated liver stiffness. It is about liver disease, not Alzheimer's disease, and does not show a treatment or cure for Alzheimer's.
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This exploratory case-control study investigates the synaptic marker beta-synuclein in serum and plasma pTau181 in adults with Down syndrome (DS) with (sDS, n = 14) and without (aDS, n = 47) clinical symptoms of Alzheimer disease (AD) as well as euploid controls (n = 23).
Why it matters
In this exploratory case-control study, serum beta-synuclein was higher in adults with Down syndrome and was more pronounced in those with clinical Alzheimer's disease symptoms. The authors highlight it as a potential early marker of Alzheimer's disease, which is about detection rather than treatment.
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These results suggest that bvFTD may be characterized by an allostatic-interoceptive overload manifested in ongoing electrophysiological markers, brain atrophy, functional networks, and cognition.
Why it matters
This study found that patients with behavioral variant frontotemporal dementia showed altered heartbeat evoked potential modulation and reduced brain volume and connectivity in the allostatic-interoceptive network compared with healthy controls and patients with Alzheimer's disease. It concerns understanding frontotemporal dementia, not treating, curing, or preventing Alzheimer's disease.
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Of 4,150 studies screened, 26 were eligible for inclusion, of which 17 were human studies, 8 were preclinical animal studies, and 1 included both human and preclinical animal studies.
Why it matters
Of 4,150 studies screened, 26 were reviewed on whether a single moderate to severe head injury leads to long-term tau build-up. Most human and animal studies suggested it does, compared with no head injury, though small samples, mostly male participants and poor control for factors like apolipoprotein E genotype call for caution. The authors suggest tau changes after injury may keep developing over time and could be a target for future treatment research.
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Cysteine-altering NOTCH3 variants identical to those causing the rare monogenic form of stroke, CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), have been reported more common than expected in the general population, but their clinical significance and contribution to stroke and dementia risk in the community remain unclear.
Why it matters
In UK Biobank whole-exome data from 200,632 people, cysteine-altering NOTCH3 variants were found in about 1 in 450 participants, more common than expected. Carriers had higher frequencies of stroke and vascular dementia compared with non-carriers, indicating these variants may contribute to these conditions in the general population.
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Aging results in gray and white matter degeneration, but the specific microglial responses are unknown.
Why it matters
This work identifies white matter-associated microglia that depend on TREM2 signaling and increase with aging. It describes an aging-related microglial state but does not test any way to treat or prevent Alzheimer's.
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Sepsis is a leading cause of death in critical illness, and its pathophysiology varies depending on preexisting medical conditions.
Why it matters
This study is about nonalcoholic fatty liver disease and sepsis, identifying NAFLD as a risk factor for sepsis and a metabolic coordination between hepatocytes and TREM2-expressing liver macrophages. It does not concern Alzheimer's disease and reports no treatment for it.
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Macrophage-mediated inflammation is critical in the pathogenesis of non-alcoholic steatohepatitis (NASH).
Why it matters
This study describes how macrophages change in a mouse model of fatty liver disease, not Alzheimer's disease. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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The discovery of TREM2 as a myeloid-specific Alzheimer's disease (AD) risk gene has accelerated research into the role of microglia in AD.
Why it matters
Using human iPSC-derived microglia and a chimeric mouse model, this study found that deleting TREM2 reduced microglial survival and impaired phagocytosis. These are laboratory and animal findings and do not establish a treatment, cure, or prevention for Alzheimer's disease in humans.
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Dementia is a rapidly rising global health crisis that silently disables families and ends lives and livelihoods around the world.
Why it matters
This review argues that microglia act as governors of neuronal function and that chronic impairment in microglia-neuron cross-talk may drive loss of synaptic and neuronal function. It notes that no early biomarkers or effective therapies exist and reports no treatment, cure or prevention.
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Hypertension is one of the main risk factors for vascular dementia and Alzheimer disease.
Why it matters
In this small study of 37 people, resting-state fMRI showed altered brain network connections in people with hypertension compared with those with normal blood pressure. It is about early brain effects of a vascular risk factor, not about treating, curing or preventing Alzheimer's disease.
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Beta-amyloid deposition is a defining feature of Alzheimer's disease (AD).
Why it matters
In postmortem human brain tissue, single-nucleus RNA sequencing found a group of CD163-positive "amyloid-responsive" microglia, the brain's immune cells, that were scarcer in people carrying APOE or TREM2 risk variants. A larger set of Alzheimer's cases confirmed that these risk variants are associated with a significant reduction in these cells. This is an observational, after-death finding about how genetic risk may shape the brain's immune response to amyloid, not evidence for any treatment.
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A hexanucleotide-repeat expansion in C9ORF72 is the most common genetic variant that contributes to amyotrophic lateral sclerosis and frontotemporal dementia 1,2 .
Why it matters
In C9orf72-mutant mice, reducing immune-stimulating gut bacteria protected against premature mortality and ameliorated systemic inflammation and autoimmunity. This is an animal study relevant to amyotrophic lateral sclerosis and frontotemporal dementia, not a demonstrated treatment, cure, or prevention for Alzheimer's disease.
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The microglial receptors CD33 and TREM2 have been associated with risk for Alzheimer's disease (AD).
Why it matters
In mice bred to build up amyloid (5xFAD), removing the microglial receptor CD33 reduced amyloid pathology and improved cognition, but only while TREM2 was present: also removing TREM2 cancelled both effects, and removing TREM2 alone worsened amyloid pathology and neurodegeneration, which CD33 removal could not rescue. Microglial genes for phagocytosis and signalling (IL-6, IL-8, acute phase response) went up without CD33 and down without TREM2, which the authors summarise as TREM2 acting downstream of CD33. These are mouse findings with no numbers given in the record; they do not show that changing CD33 or TREM2 would treat or prevent Alzheimer's disease in people.
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Alzheimer's disease (AD) is a progressive neurodegenerative disease in which the formation of extracellular aggregates of amyloid beta (Aβ) peptide, fibrillary tangles of intraneuronal tau and microglial activation are major pathological hallmarks.
Why it matters
This study found that galectin-3 is elevated in Alzheimer's brains and that deleting it in 5xFAD mice attenuated microglial activation. These are mouse and human tissue findings and do not establish a treatment, cure, or prevention for Alzheimer's disease in people.
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While cytoplasmic aggregation of TDP-43 is a pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia, how aggregates form and what drives its nuclear clearance have not been determined.
Why it matters
In cells, TDP-43 formed liquid droplets in the cytoplasm that turned into gels or solids and led to blocked nuclear transport, loss of nuclear TDP-43 and cell death. This is a laboratory cell study of how TDP-43 aggregates may harm neurons, not a treatment or prevention tested in 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.
- Lower Retinal Arteriolar Density Is Associated With Higher Cerebral Small Vessel Disease Burden: An Optical Coherence Tomography Angiography Study
- Lysosome dysfunction as a cause of neurodegenerative diseases: Lessons from frontotemporal dementia and amyotrophic lateral sclerosis
- Genetic analysis of Down syndrome facilitated by mouse chromosome engineering
- HIV-1, macrophages, glial cells, and cytokines in AIDS nervous system disease
- Extracellular deposits of A beta produced in cultures of Alzheimer disease brain vascular smooth muscle cells
- Reelin and ApoE receptors cooperate to enhance hippocampal synaptic plasticity and learning
- Role of increased cerebral myo-inositol in the dementia of Down syndrome
- The A53T alpha-synuclein mutation increases iron-dependent aggregation and toxicity
- Associations of plasma SMOC1 and soluble IL6RA levels with the progression from mild cognitive impairment to dementia
- Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges