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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Participants' median age was 70.7 years (Q1-Q3 = 67.8-74.0), with 52.4% being women.
Why it matters
In this cross-sectional study, insomnia symptoms and early rising were associated with larger white matter hyperintensity volume and smaller hippocampal volume. Because it is cross-sectional, it cannot show whether sleep problems cause these brain changes or whether treating sleep would help.
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). Moreover, 12 proteins related to endothelial function and inflammation were associated with neuroimaging features of SVD.
Why it matters
This study found that 12 proteins related to endothelial function and inflammation were associated with neuroimaging features of small vessel disease, and 5 of 13 proteins were linked to risk of all-cause dementia or stroke. The findings suggest potential therapeutic targets and pathways, but no treatment was tested in this cross-sectional analysis.
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A total of 110 participants (mean [SD] age, 67.9 [4.6] years; 68 female [61.8%]) were randomized to the experimental group (n = 55) and the sham group (n = 55) and included in the intention-to-treat analysis.
Why it matters
In this trial of 110 older adults with sleep disorders and mild cognitive impairment, combining repetitive transcranial magnetic stimulation with tai chi improved sleep quality and cognitive test scores compared to a sham group. These findings suggest a non-drug approach may help delay or prevent mild cognitive impairment, though longer-term benefits are not yet known.
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Microglia are crucial for maintaining brain health and neuron function.
Why it matters
This study reports that microglia connect to neurons through tunneling nanotubes and can remove toxic tau and alpha-synuclein aggregates, restoring neuronal health in lab conditions. It is early experimental work and does not show a treatment, cure or prevention for Alzheimer's in people.
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CSF sTREM2 levels are positively associated with an increased risk of AD and MCI.
Why it matters
Combining thirty-six studies, this meta-analysis found that sTREM2, a marker of brain immune activity, was higher in spinal fluid of people with Alzheimer's and with mild cognitive impairment than in healthy controls, and higher blood levels were linked to Alzheimer's. However, levels did not separate the two stages. The authors see plasma sTREM2 as a possible diagnostic marker that needs long-term follow-up studies.
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Mediterranean diets may be neuroprotective and prevent cognitive decline relative to Western diets; however, the underlying biology is poorly understood.
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Triggering receptor expressed on myeloid cells-2 (TREM2) and progranulin (PGRN) are critical regulators of microglia activation and can be detected in cerebrospinal fluid (CSF).
Why it matters
In 663 participants, microglial reactivity measured by cerebrospinal fluid sTREM2 and PGRN was related to presynaptic loss independently of amyloid and tau, though whether microglial reactivity helps or harms in Alzheimer's remains debated. It is a biomarker association study, so it does not show a treatment, cure or prevention.
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57/100
Choosing optimal P2Y12 inhibitor in frail older adults is challenging because they are at increased risk of both ischemic and bleeding events.
Why it matters
This study examined which antiplatelet drugs frail older adults receive after a heart attack and found that frailty was linked to lower odds of getting newer, stronger drugs. It is about heart attack care, not about treating, curing, or preventing Alzheimer's disease.
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Microglial activation occurs early in Alzheimer's disease (AD) and previous studies reported both detrimental and protective effects of microglia on AD progression.
Why it matters
In 402 patients, cerebrospinal fluid sTREM2 was associated with amyloid-related p-tau increases and glucose hypermetabolism, and the authors note that microglia have been reported to have both detrimental and protective effects on Alzheimer's disease progression. This is a cross-sectional study, so it cannot show whether microglial activation causes or protects against disease progression.
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Plasma GFAP alone differentiates AD from FTD and neurodegenerative dementias from HC but with lower accuracy than p-tau181 and NfL.
Why it matters
In a clinical cohort, plasma p-tau181 distinguished frontotemporal dementia from Alzheimer's disease, and plasma neurofilament light distinguished degenerative dementias from healthy controls. These biomarkers aid diagnosis and do not treat, cure, or prevent Alzheimer's disease.
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Microglia and complement can mediate neurodegeneration in Alzheimer's disease (AD).
Why it matters
In Tau P301S mouse models, this study found that astrocytes and microglia eliminate synapses in a C1q-dependent manner. These are mouse findings and do not establish a treatment, cure, or prevention for Alzheimer's disease in humans.
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Fused in sarcoma (FUS) is an RNA-binding protein that is genetically and pathologically associated with rare and aggressive forms of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
Why it matters
In FUS mutant mice, the antisense oligonucleotide ION363 silenced Fus and delayed motor neuron degeneration, and one patient with ALS with a FUSP525L mutation received preliminary evidence of reduced FUS levels after repeated intrathecal infusions. This is an animal and single-patient preliminary study relevant to FUS-dependent ALS and frontotemporal dementia, not a demonstrated treatment, cure, or prevention for Alzheimer's disease.
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2-Deoxy-2-[ 18 F]fluoro-d-glucose positron emission tomography (FDG-PET) is widely used to study cerebral glucose metabolism.
Why it matters
In mice, this study found that the brain's immune cells (microglia) take up more glucose than neurons or astrocytes. Changes in microglial glucose uptake accounted for both a drop in the FDG-PET brain-scan signal in Trem2-deficient mice and a rise in mice modelling amyloid build-up. This suggests an FDG-PET scan partly reflects immune-cell activity and not only neuron activity. It concerns how a scan signal is produced and is not a way to treat, cure or prevent Alzheimer's disease.
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Alzheimer's disease (AD) is associated with abnormal tau and amyloid-β accumulation in the brain, leading to neurofibrillary tangles, neuropil threads and extracellular amyloid-β plaques.
Why it matters
This mRNA-seq study of post-mortem brain samples identified differentially expressed genes in Alzheimer's disease, including microglia gene OLR1 and astrocyte gene CDK2AP1. It is a gene expression study and does not report a treatment or cure.
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No treatment for frontotemporal dementia (FTD), the second most common type of early-onset dementia, is available, but therapeutics are being investigated to target the 2 main proteins associated with FTD pathological subtypes: TDP-43 (FTLD-TDP) and tau (FTLD-tau).
Why it matters
This work tested truncated stathmin-2 as a possible marker to tell apart two subtypes of frontotemporal dementia, FTLD-TDP and FTLD-tau, which current trials cannot distinguish. The findings come from cells grown in the lab, so it is early research and does not yet show a treatment or cure.
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57/100
There are few validated fluid biomarkers in frontotemporal dementia (FTD).
Why it matters
This study measured plasma GFAP and neurofilament light chain in people with genetic forms of frontotemporal dementia and found GFAP was raised in those with progranulin-associated disease. It is a biomarker study only and does not test any treatment, cure, or prevention for dementia.
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While delirium is associated with cognitive decline and dementia, there is limited evidence to support causality for this relationship.
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Our study compared the pain associated with 5- and 15-s subcutaneous injections of gantenerumab and evaluated the tolerability and pharmacokinetic properties of subcutaneous gantenerumab.
Why it matters
This phase 1 study in healthy volunteers only looked at pain, tolerability, and blood levels of gantenerumab given by subcutaneous injection. It provides no evidence about treating, curing, or preventing Alzheimer's disease.
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Neuronal and synaptic loss is characteristic in many neurodegenerative diseases, such as frontotemporal dementia and Alzheimer's disease.
Why it matters
In two mouse models of neurodegeneration, daily gamma entrainment preserved neuronal and synaptic density and modified cognitive performance. It is animal research, so it does not yet show any treatment, cure or prevention for Alzheimer's disease.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial surface receptor genetically linked to the risk for Alzheimer's disease (AD).
Why it matters
In 5xFAD mice, a model of Alzheimer's disease, raising soluble TREM2 in the brain by direct injection or by a viral vector "reduces amyloid plaque load and rescues functional deficits of spatial memory and long-term potentiation". The study also reports that soluble TREM2 increased microglial proliferation, migration and clustering around plaques, and their "uptake and degradation of Aβ". These are mouse results with no sample sizes or effect sizes given here. They do not show that soluble TREM2, or any TREM2-targeting drug, treats or prevents Alzheimer's disease in people.
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LBD patients with AD copathology harbor greater neocortical SYN pathology.
Why it matters
In people with Lewy body disorders, those who also had Alzheimer's disease pathology had more alpha-synuclein pathology in the brain and did worse on a naming task. This is an autopsy study describing how co-occurring pathologies relate to thinking problems, not a treatment or cure.
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Animal models of adult-onset neurodegenerative diseases have enhanced the understanding of the molecular pathogenesis of Alzheimer's disease, Parkinson's disease, frontotemporal dementia, and amyotrophic lateral sclerosis.
Why it matters
This review discusses the limitations and utility of rodent models of Alzheimer's disease and other neurodegenerative diseases and calls for models that more faithfully recapitulate human disease. It reports no treatment effect and no cure or prevention.
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Reliable biomarkers of frontotemporal dementia (FTD) are currently lacking.
Why it matters
This study investigated whether cerebrospinal fluid sTREM2 levels differ between frontotemporal dementia and controls and across clinical and genetic subtypes. It is about frontotemporal dementia, so it does not provide evidence about treating, curing or preventing Alzheimer's disease.
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The triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial innate immune receptor associated with a lethal form of early, progressive dementia, Nasu-Hakola disease, and with an increased risk of Alzheimer's disease.
Why it matters
In mice, absence of Trem2 impaired synapse elimination during early brain development, with enhanced excitatory neurotransmission and reduced long-range connectivity. It is animal work on brain development and does not test an Alzheimer's treatment or cure.
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Mutations in triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to increased Alzheimer's disease (AD) risk.
Why it matters
In lab and mouse experiments, the microglial receptor TREM2, a gene linked to higher Alzheimer's risk, bound directly to small clumps of amyloid-beta (oligomers) "with nanomolar affinity", while Alzheimer's-associated TREM2 mutations reduced that binding. Without TREM2, microglia broke down less amyloid-beta in culture and in mouse brain, and many of their responses to amyloid-beta (cytokine release, migration, proliferation, shape changes) depended on TREM2. This describes a possible mechanism in cells and mice; it did not involve patients or test a treatment.
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.
- The synaptic accumulation of hyperphosphorylated tau oligomers in Alzheimer disease is associated with dysfunction of the ubiquitin-proteasome system
- Plasma p-tau217 as a biomarker of Alzheimer's disease pathology in individuals with Down syndrome
- Impact of Reference and Target Region Selection on Amyloid PET SUV Ratios in the Phase 1b PRIME Study of Aducanumab
- Cognitive decline and brain volume loss as signatures of cerebral amyloid-beta peptide deposition identified with Pittsburgh compound B: cognitive decline associated with Abeta deposition
- Prion-like properties of pathological TDP-43 aggregates from diseased brains
- Performance of plasma phosphorylated tau 181 and 217 in the community
- Classification of tauopathies from human brain homogenates through salt-modulated tau amplification
- Increased risk of late posttraumatic seizures associated with inheritance of APOE epsilon4 allele
- The cholinergic system and Parkinson disease
- Therapeutic reduction of ataxin-2 extends lifespan and reduces pathology in TDP-43 mice