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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We evaluated whether insomnia symptom severity was associated with cognitive function, and whether this relationship was modified by biomarkers associated with Alzheimer's disease risk.
Why it matters
This study evaluated whether insomnia symptom severity is linked to cognitive function and whether this relationship is modified by APOE genotype. It found that more severe insomnia symptoms were associated with lower performance on global cognition and memory recall.
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Genetic and genome-wide association studies suggest a central role for microglia in Alzheimer's disease (AD).
Why it matters
This study used single-cell RNA sequencing of microglia from different mouse strains with and without APP/PS1 to show that genetic diversity alters microglial features and responses to amyloidosis. It is animal research on microglial heterogeneity and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Triggering receptor expressed on myeloid cells 2 (TREM2), a receptor exclusively expressed by microglia in the brain, modulates microglial immune homeostasis.
Why it matters
In aged mice, loss of TREM2 was linked to resilience to synaptic and cognitive impairment, which is unexpected given that TREM2 loss-of-function mutations raise Alzheimer's risk in humans. This is animal work and does not establish a treatment or prevention for Alzheimer's disease.
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The Trem2 variant R47H, confers substantially elevated risk of developing late onset Alzheimer's disease, while NHD-linked Trem2 variants like Y38C, are associated with development of early onset dementia with white matter pathology.
Why it matters
In a novel mouse model, the Trem2 Y38C variant or loss of Trem2 impaired neuronal synapses in adult mice. This is an animal study, so it does not establish whether these synaptic changes occur in people or whether they can be treated.
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Triggering receptor expressed on myeloid cells-2 (TREM2) is an immune receptor expressed on microglia that also can become soluble (sTREM2).
Why it matters
This biophysical study used biolayer interferometry to examine how TREM2 and soluble TREM2 interact with apolipoprotein E and monomeric amyloid beta. It is an in-vitro laboratory analysis of molecular binding and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a receptor mainly expressed on the surface of microglia.
Why it matters
This review describes TREM2 as a microglial receptor with a long ectodomain that interacts with the extracellular environment and has been found to play a role in Alzheimer's disease. It reports no treatment, cure, or prevention.
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Depression and dementia are major public health problems.
Why it matters
This review discusses the role of adult hippocampal neurogenesis as a possible shared mechanism linking major depressive disorder and Alzheimer's disease. It states that no effective drug is available to treat Alzheimer's disease and that the biological connection between depression and Alzheimer's disease remains unclear.
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Thalamic atrophy is a common feature across all forms of FTD but little is known about specific nuclei involvement.
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ApoE4 impairs pericyte-mediated basement membrane formation, potentially contributing to the cerebrovascular effects of apoE4.
Why it matters
In mice with different human APOE versions, apoE4 in brain pericytes impaired basement membrane formation and increased plasma protein leakage compared with apoE3. This is animal research on a possible amyloid-independent effect of apoE4 and does not show any treatment for people.
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Tauopathies are a heterogenous class of diseases characterized by cellular accumulation of aggregated tau and include diseases such as Alzheimer's disease (AD), progressive supranuclear palsy and chronic traumatic encephalopathy.
Why it matters
This review describes how tau pathology, synapse loss and reactive microglia are linked in diseases including Alzheimer's. It summarizes disease processes rather than testing any treatment, cure or prevention.
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Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB) are clinically and neuropathologically highly related α-synucleinopathies that collectively constitute the second leading cause of neurodegenerative dementias.
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the studies reviewed show that VD contributes to cerebral activity in both embryonic and adult brain, helping the connectivity of neural circuits responsible for locomotor, emotional and reward-dependent behavior.
Why it matters
This review found low vitamin D levels in people with Alzheimer's and other neurological conditions, but notes the findings are controversial and mostly from observational studies with few and conflicting interventional studies. It concludes the role of vitamin D in neurological disease is mostly unclear and that randomized trials are needed, so it does not support vitamin D supplementation as a treatment.
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Cerebral small vessel disease (cSVD) comprises pathological processes of the small vessels in the brain that may manifest clinically as stroke, cognitive impairment, dementia, or gait disturbance.
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PSEN2 (presenilin 2) is one of the 3 proteins that, when mutated, causes early onset familial Alzheimer disease (FAD) cases.
Why it matters
In cell models, mutated presenilin 2 linked to familial Alzheimer's disease blocked autophagy by disrupting the fusion of autophagosomes with lysosomes. This is laboratory cell research, so it does not yet show a treatment, cure, or prevention for people.
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Increasing evidences support the notion that the impairment of intracellular degradative machinery is responsible for the accumulation of oxidized/misfolded proteins that ultimately results in the deposition of protein aggregates.
Why it matters
In a mouse model of Down syndrome, intranasal rapamycin restored mTOR signaling and reduced oxidative damage to specific proteins. This is an animal study, so it does not show that rapamycin treats or prevents Alzheimer's disease in people.
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Alzheimer's disease (AD) is a heterogeneous disorder with multiple etiologies.
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Type I interferons (IFN-I) are the principal antiviral molecules of the innate immune system and can be made by most cell types, including central nervous system cells.
Why it matters
In a mouse prion disease model, chronic neurodegeneration induced type I interferon via STING, shaping microglial phenotype and accelerating disease progression. This is animal work in a different disease and does not establish an Alzheimer's treatment.
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45/100
Air pollution is a risk factor for cardiovascular and respiratory morbidity and mortality.
Why it matters
This paper proposes that air pollutants such as particulate matter and ozone can activate the stress hormone system, which may contribute to brain conditions including dementia. It is a conceptual review of a possible pathway, not evidence that reducing pollution treats or prevents Alzheimer's disease.
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A chronic and gradual increase in pulse pressure (PP) is associated with cognitive decline and dementia in older individuals, but the mechanisms remain ill-defined.
Why it matters
In mice, six weeks of high pulse pressure caused brain microvascular endothelial dysfunction, neurovascular unit damage, and cognitive decline in both wild-type and APP/PS1 mice. This is animal research and does not show a treatment, cure, or prevention for Alzheimer's disease in people.
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A diffusion prepared 3D GRASE pCASL sequence with TGV regularized SPA modeling was proposed to measure BBB water permeability noninvasively with good reproducibility. k w may serve as an imaging marker of cerebral SVD and associated cognitive impairment.
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Alzheimer´s disease (AD) is a devastating neurodegenerative disease of the elderly population.
Why it matters
This review describes how γ-secretase cuts amyloid precursor protein within its transmembrane domain to release amyloid β peptides of 37-43 amino acids, including the longer pathogenic forms. It is a summary of existing knowledge and does not itself provide a treatment, cure, or prevention.
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Hippocampal involvement in MDD is confined to principal substructures only.
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Synaptic dysfunction plays a central role in Alzheimer's disease (AD), since it drives the cognitive decline.
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Systemic inflammation can impair cognition with relevance to dementia, delirium and post-operative cognitive dysfunction.
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45/100
This study aimed to investigate the effects of triggering receptor expressed on myeloid cell-2 (TREM2) on the production of pro-inflammatory mediators and cytokines induced by lipopolysaccharide (LPS) in BV2 microglia.
Why it matters
In BV2 microglia cells, TREM2 overexpression or silencing affected lipopolysaccharide-induced inflammatory mediators and cytokines, with involvement of PI3K/NF-κB signaling. This is cell-culture research and does not show any treatment, cure or prevention for 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.
- Repulsive Guidance Molecule-A as a Therapeutic Target Across Neurological Disorders: An Update
- Associations of plasma von Willebrand Factor levels with cognitive decline and neurodegeneration in older adults without dementia
- Progressive supranuclear palsy pathology caused by a novel silent mutation in exon 10 of the tau gene: expansion of the disease phenotype caused by tau gene mutations
- Formation and function of apolipoprotein E-containing lipoproteins in the nervous system
- Increase in hippocampal volume after electroconvulsive therapy in patients with depression: a volumetric magnetic resonance imaging study
- Low-dose intranasal deferoxamine modulates memory, neuroinflammation, and the neuronal transcriptome in the streptozotocin rodent model of Alzheimer’s disease
- β-Hydroxybutyrate inhibits inflammasome activation to attenuate Alzheimer's disease pathology
- Synaptosomal‐Associated Protein 25 kDA (SNAP‐25) Levels in Cerebrospinal Fluid: Implications for Alzheimer's Disease Diagnosis and Monitoring
- LILRB2-mediated TREM2 signaling inhibition suppresses microglia functions
- Structural neuroimaging in Altheimer's disease: do white matter hyperintensities matter?