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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'Sundowning' in dementia and Alzheimer's disease is characterized by early-evening agitation and aggression.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is an orphan immune receptor expressed on cells of myeloid lineage such as macrophages and microglia.
Why it matters
In a mouse model carrying the Alzheimer's risk variant Trem2 R47H, activating antibodies were used to study effects on myeloid cell function. This is animal and cell-level work and does not show any benefit for treating or preventing Alzheimer's disease in people.
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In vivo [ 18 F]-AV-1451 PET neuroimaging was performed in 5 patients with sporadic CJD (median age, 66 years [63-74]), and results were compared to cognitively normal (CN) persons (n = 44; median age, 68 years [63-74]) and to participants with very mild Alzheimer disease (AD) dementia (n = 8; median age, 77 years [63-90]).
Why it matters
This small imaging study of 5 patients with autopsy-confirmed Creutzfeldt-Jakob disease found tau-PET patterns that differed from Alzheimer's disease. It is about distinguishing these diseases on scans, not about treating or preventing Alzheimer's.
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See Attems and Jellinger (doi:10.1093/brain/awx360) for a scientific commentary on this article.
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Early life experience influences stress reactivity and mental health through effects on cognitive-emotional functions that are, in part, linked to gene expression in the dorsal and ventral hippocampus.
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Dendritic spine structure is defined by filamentous actin (F-actin) and we observed depolymerization of synaptosomal F-actin accompanied by increased globular-actin (G-actin) at as early as 1 month of age in a mouse model of AD (APPswe/PS1ΔE9, male mice).
Why it matters
This study in a mouse model of Alzheimer's disease found that disassembly of F-actin in dendritic spines occurred very early, before the onset of pathological hallmarks, and contributed to behavioral dysfunction. It also observed decreased synaptosomal F-actin in postmortem brain from people with mild cognitive impairment and Alzheimer's disease.
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Major Depressive Disorder (MDD) is a common psychiatric disorder for which available medications are often not effective.
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Alzheimer's disease (AD) is characterized by a progressive cognitive decline and believed to be driven by the self-aggregation of amyloid-β (Aβ) peptide into oligomers and fibrils that accumulate as senile plaques.
Why it matters
This study compared how microglia cultured for different lengths of time respond to beta-amyloid stimulation. It is an in-vitro laboratory study, so it does not show any treatment, cure or prevention for Alzheimer's disease in people.
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The mammalian target of rapamycin (mTOR) is a serine/threonine protein kinase involved in the regulation of protein synthesis and degradation, longevity and cytoskeletal formation.
Why it matters
People with Down syndrome have an extra copy of chromosome 21, which carries several genes involved in forming the amyloid plaques and tau tangles of Alzheimer's disease. This review gathers earlier research suggesting that overactive mTOR signalling, a growth-control pathway in cells, contributes to both, and that oxidative stress "may significantly contribute" to that link. It is a review of mechanisms, not a trial, and reports no treatment or prevention result.
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The use of Panax ginseng and Panax quinquefolius in traditional Chinese medicine dates back to about 5000 years ago thanks to its several beneficial and healing properties.
Why it matters
This review states that preclinical and clinical evidence supports beneficial effects of Panax ginseng and Panax quinquefolius in diseases including dementia. It provides an overview of these plants and their safety, but does not establish that they treat or prevent Alzheimer's disease.
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It is increasingly recognized that obesity is a risk factor for microvascular disease, involving both structural and functional changes in the microvasculature.
Why it matters
This review proposes that obesity-related microvascular dysfunction, involving endothelial dysfunction and impaired organ perfusion, is a common pathway that predisposes to conditions including microvascular dementia. It is a mechanistic review and does not test whether treating obesity or microvascular disease prevents dementia.
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Although multiple CHCHD10 mutations are associated with the spectrum of familial and sporadic frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS) diseases, neither the normal function of endogenous CHCHD10 nor its role in the pathological milieu (that is, TDP-43 pathology) of FTD/ALS have been investigated.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder, accompanied by memory loss and cognitive impairments, and there is no effective treatment for it at present.
Why it matters
In a rat model of Alzheimer-like changes, a dual GLP-1/GIP receptor agonist prevented spatial learning deficits and reduced phosphorylated tau, brain inflammation, and apoptosis while re-sensitizing insulin signaling. This is an animal study and does not show that the drug treats, cures, or prevents Alzheimer disease in people.
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45/100
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that lacks a predictive and broadly applicable biomarker.
Why it matters
This study used a transcriptome-driven approach to develop noninvasive prognostic biomarkers for progression of amyotrophic lateral sclerosis. It is about ALS, not Alzheimer's disease, so it has no implications for treating, curing or preventing Alzheimer's.
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LP can be safely performed to study CSF biomarkers in DS.
Why it matters
Among 80 adults with Down syndrome who had a lumbar puncture, 90% had no adverse events and the most common problem was headache. This suggests lumbar puncture is feasible for studying Alzheimer's biomarkers in this population, though it only addresses the safety of the procedure, not treatment.
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Neuroinflammation and activation of innate immunity are early events in neurodegenerative diseases including Alzheimer's disease (AD).
Why it matters
In APP/PS1 transgenic mice, TREM2 was found to be involved in inflammation, neuronal cell survival and neurogenesis. This is early animal work and does not show that any treatment prevents or cures Alzheimer's disease in people.
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Alzheimer's disease (AD) is the leading cause of dementia and mitigating amyloid-β (Aβ) levels may serve as a rational therapeutic avenue to slow AD progression.
Why it matters
This laboratory study found that ROCK1 protein levels were elevated in mild cognitive impairment due to Alzheimer's disease and Alzheimer's brains, and that depleting ROCK1 or ROCK2 reduced amyloid-β production in neurons and in ROCK1 heterozygous knock-out mice. It is early mechanistic work supporting ROCK1 and ROCK2 as possible therapeutic targets, not a proven treatment or cure.
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There is significant evidence that pathways involving inflammation and oxidative-nitrosative stress (ONS) play a key pathophysiological role in promoting cognitive dysfunction.
Why it matters
This paper states there is significant evidence that inflammation and oxidative-nitrosative stress play a key pathophysiological role in promoting cognitive dysfunction. It does not report any treatment, cure or prevention for Alzheimer's disease.
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The colony-stimulating factor-1 receptor (CSF-1R) kinase regulates tissue macrophage homeostasis, osteoclastogenesis, and Paneth cell development.
Why it matters
This review reports that in mice, CSF-1R signaling controls development and maintenance of microglia and regulates neuronal differentiation and survival, and notes an inherited adult-onset progressive dementia linked to inactivating mutations in this pathway. It reports no treatment or prevention result for Alzheimer's disease.
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Alzheimer's disease (AD) is associated with the accumulation of β-amyloid (Aβ) as senile plaques in the brain, thus leading to neurodegeneration and cognitive impairment.
Why it matters
In a mouse model, chronic Toxoplasma gondii infection enhanced the clearance of beta-amyloid by recruited monocytes. This is early animal work on infection and plaque removal, and it does not show that any treatment prevents or cures Alzheimer's disease in people.
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Kir4.1 is an inwardly rectifying K(+) channel expressed exclusively in glial cells in the central nervous system.
Why it matters
This review covers the glial potassium channel Kir4.1 and its roles in the central nervous system, noting that knocking it out in rodents causes severe neurological deficits. It provides no treatment, cure or prevention for Alzheimer's disease.
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Alzheimer's disease (AD), the most common cause of dementia in the elderly, is a complex neurodegenerative disease marked by the appearance of amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles.
Why it matters
This review reports that variants in the microglial-expressed receptor TREM2 are associated with a 2-4-fold increased risk of developing Alzheimer's disease. It summarizes research on whether loss of TREM2 function matters but offers no treatment or cure.
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Frontotemporal dementia (FTD) refers to a group of clinically and genetically heterogeneous neurodegenerative disorders that are a common cause of adult-onset behavioural and cognitive impairment.
Why it matters
This review covers genetic mutations linked to frontotemporal dementia and its movement symptoms, including genes for tau and progranulin. It reports no treatment, cure, or prevention for Alzheimer's disease.
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Esophageal cancer is often diagnosed at an advanced stage.
Why it matters
This study is about esophageal cancer, not Alzheimer's disease, so it has no direct meaning for treating, curing or preventing Alzheimer's. It identified genes differentially expressed in esophageal cancer for diagnostic marker purposes.
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Stress granules (SGs) are RNA-containing cytoplasmic foci formed in response to stress exposure.
Why it matters
This paper discusses stress granules and their link to neurodegenerative diseases such as ALS and frontotemporal dementia, not Alzheimer's disease. It does not report 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.
- Transcriptome-informed metabolic modeling reveals astrocyte-specific vulnerabilities in mild cognitive impairment and Alzheimer’s disease progression
- Aluminium toxicosis: a review of toxic actions and effects
- Altered glymphatic function and cerebrovascular reactivity in white matter hyperintensities: Insights into cognitive impairment
- Metformin protects against insulin resistance-related dementia risk involving restored microglial homeostasis
- Testing the Association Between Neighborhood Disadvantage and White Matter Hyperintensities
- Frequency and Clinical Outcomes Associated With Tau Positron Emission Tomography Positivity
- Influence of HAART on HIV-related CNS disease and neuroinflammation
- Glial dysfunction in the pathogenesis of α-synucleinopathies: emerging concepts
- Transplanted neural-like cells improve memory and Alzheimer-like pathology in a rat model
- Modifiers of C9orf72 dipeptide repeat toxicity connect nucleocytoplasmic transport defects to FTD/ALS