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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Chronic exposure to increased glucocorticoid concentrations appears to lower the threshold for hippocampal neuronal degeneration in the old rat.
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The appearance of inflammatory markers associated with amyloid plaques indicates a state of chronic inflammation in Alzheimer's disease (AD).
Why it matters
In human cells, the inflammatory cytokines TNFalpha and IFNgamma increased production of beta-amyloid peptides and reduced secretion of soluble APPs. This suggests inflammation can alter amyloid precursor protein metabolism, but it is cell-based work and does not show that anti-inflammatory drugs treat or prevent Alzheimer's disease in people.
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Microglia-mediated inflammatory responses have been implicated in the pathogenesis of neuritic plaques in Alzheimer's disease.
Why it matters
This study examined interleukin-1 alpha-immunoreactive microglia in the brains of 20 neurologically normal people aged 2 to 80 and found that enlarged, phagocytic microglia increase with age. It suggests that normal aging events may promote inflammatory responses relevant to Alzheimer's disease, but it did not test any treatment or prevention.
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The neural protein FE65 contains two types of protein-protein interaction modules: one WW binding domain and two phosphotyrosine binding domains.
Why it matters
This laboratory study identified proteins that bind to a specific domain of the neural protein FE65, which itself interacts with the amyloid precursor protein. It describes a basic protein interaction and does not test any treatment, prevention or cure for Alzheimer's disease.
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Genetic variation in the APOE gene and variation in chromosome 21 genotypes, including the APP locus, may influence age-associated cognitive decline in adults with Down syndrome.
Why it matters
In 41 adults with Down syndrome, genetic variability at APOE and APP was not significantly associated with cognitive decline, while unusual allelic variability at D21S11 was seen in older individuals without decline. These findings are discussed as hypotheses and do not establish a treatment or prevention.
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Circulating PSA producing cells were present in 29 of 33 patients (88 percent) with metastatic prostate cancer.
Why it matters
This study found that polymerase chain reaction based assays offered no immediate benefit for preoperative prostate cancer staging, with no statistically significant relationship of a positive PSA polymerase chain reaction signal to pathological stage, tumor grade, apical involvement or positive surgical margins. The prognostic significance of detecting circulating prostate specific signals awaits longer followup.
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Detailed molecular pathology studies and clinicopathological phenotyping of familial amyotrophic lateral sclerosis (FALS) with characterised mutations in the gene encoding Cu/Zn superoxide dismutase (SOD1) will yield important insights into the pathogenesis of motor neuron degeneration.
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Mutations in the human Cu,Zn superoxide dismutase gene (SOD1) are found in 20% of kindreds with familial amyotrophic lateral sclerosis.
Why it matters
Transgenic mice expressing a mutant human SOD1 developed neurofilament-rich inclusions in spinal motor neurons resembling those in ALS, while mice with wild-type human SOD1 did not. This is an animal model of ALS-related pathology and does not test any treatment or prevention for Alzheimer's disease.
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45/100
Phorbol esters, activators of protein kinase C (PKC), regulate the relative utilization of alternative processing pathways for the Alzheimer beta-amyloid precursor protein (beta-APP) in intact cells, increasing the production of nonamyloidogenic soluble beta-APP (s beta-APP) and decreasing that of neurotoxic beta-amyloid (A beta) peptide.
Why it matters
In a cell-free system, protein kinase C activation increased formation of secretory vesicles containing beta-APP from the trans-Golgi network. This is a laboratory mechanism study and does not show that this pathway can treat, cure, or prevent Alzheimer's disease.
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Stimulation of muscarinic m1 or m3 receptors can, by generating diacylglycerol and activating protein kinase C, accelerate the breakdown of the amyloid precursor protein (APP) to form soluble, nonamyloidogenic derivatives (APPs), as previously shown.
Why it matters
In cell and rat neuron experiments, stimulating metabotropic glutamate receptors sped up processing of amyloid precursor protein into nonamyloidogenic fragments. This is early laboratory work and does not show a treatment, cure, or prevention for Alzheimer's disease.
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In Alzheimer disease, a combination of genetic predisposition and environmental factors may contribute to changes in beta-amyloid precursor protein (APP) expression, beta-amyloid peptide deposition, and neuronal loss.
Why it matters
In mice, peripheral stimulation with lipopolysaccharide triggered a transient rise in inflammatory cytokine mRNAs followed by changes in amyloid precursor protein isoform expression in the cerebellum but not the cerebral cortex. These animal findings suggest inflammation may alter APP processing but do not demonstrate any treatment or prevention for Alzheimer's disease.
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The Alzheimer amyloid precursor protein (APP) undergoes complex processing resulting in the production of a 4-kDa amyloid peptide (A beta) which has been implicated in the pathogenesis of Alzheimer's disease.
Why it matters
Using human NT2N neurons, this study examined how muscarinic receptors and related signaling pathways affect secretion of amyloid precursor protein and production of amyloid beta. It is cell-based laboratory work and reports no treatment, cure or prevention.
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Microtubule-associated protein tau is abnormally hyperphosphorylated in the brain of patients with Alzheimer disease and in this form is the major protein subunit of the paired helical filaments (PHF), the most prominent lesion of the disease.
Why it matters
This laboratory study examined how two brain protein phosphatases dephosphorylate tau in paired helical filaments, the main lesion of Alzheimer disease. It is basic biochemical work on tau and does not test any treatment, cure, or prevention in people.
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Despite increasing evidence for a pathogenetic role for the beta-amyloid precursor protein (beta APP) in Alzheimer disease, the physiological function of the protein remains unclear.
Why it matters
In P19 mouse embryonal carcinoma cells, beta APP695 expression increased during retinoic acid-induced neuronal differentiation without secretory cleavage. This is a basic cell study of protein expression and offers no treatment, cure or prevention for Alzheimer disease.
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To investigate the role of proteolysis in amyloid formation, we studied the localization of the proteolytic enzymes, cathepsin D and cathepsin B, in the prefrontal cerebral cortex and hippocampus of human postmortem brains from patients with Alzheimer's disease and from individuals free of neurological disease.
Why it matters
This postmortem brain study found cathepsin D and cathepsin B concentrated within senile plaques in Alzheimer's disease, suggesting a neuronal origin. It is observational tissue analysis and does not test any treatment, cure or prevention.
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A comprehensive language test battery (Aachen Aphasia Test) was administered to 45 patients in the early, middle or later stages of Huntington's disease (HD) and to 20 control subjects.
Why it matters
In 45 patients with Huntington's disease, language problems such as naming errors appeared to come mainly from visual misperception and movement-related speech difficulties rather than primary language changes. This concerns Huntington's disease and does not address treating, curing or preventing Alzheimer's disease.
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Deposits of amyloid fibers are found in large numbers in the walls of blood vessels and in neuritic plaques in the brains of patients with Alzheimer disease and adults with Down syndrome.
Why it matters
This study identified and cloned a gene encoding the amyloid peptide found in Alzheimer's brain deposits and located it on human chromosome 21. It provides a possible genetic link between Alzheimer's disease and Down syndrome but does not itself offer a treatment or cure.
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BackgroundSystemic inflammation has been implicated in cognitive aging and neurodegeneration; however, inflammatory biomarkers are expressed in coordinated patterns rather than as isolated markers.
Why it matters
In Black midlife and older adults, two groups of inflammatory plasma biomarkers were inversely associated with cognitive performance, mainly among participants aged 45 to under 65. This is a cross-sectional study of associations and does not test any treatment, cure, or prevention.
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ObjectivePlasma p-Tau217 leaves 30-50% of patients in an indeterminate "gray zone" often requiring A{beta}-PET.
Why it matters
This study developed a two-stage plasma biomarker model that classified more participants without amyloid PET and reduced modeled testing costs compared with p-Tau217 screening with PET confirmation of the gray zone. It concerns diagnostic testing strategy, not treating, curing or preventing Alzheimer's disease.
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Non-core NfL and GFAP biomarkers are associated with both cross-sectional and longitudinal cognitive performance.
Why it matters
In a community-based cohort of Black adults, higher brain-derived phosphorylated tau 181 was cross-sectionally associated with poorer MoCA score, and higher neurofilament light chain with lower PACC score. Longitudinal associations over one year were also examined, but this is observational work on biomarker-cognition links, not a treatment or prevention study.
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Among 45,651 patients, 311 delirium events occurred among continuous users and 84 among early discontinuers, corresponding to incidence rates of 66 and 112 events per 10,000 person-years, respectively.
Why it matters
In this large Danish register study, continuous use of acetylcholinesterase inhibitors was associated with a lower risk of delirium compared with early discontinuation. The findings support maintaining this therapy in routine dementia care, though the study design cannot prove that the drugs themselves caused the lower risk.
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44/100
Alterations in synaptic homeostasis are linked to cognitive and behavioural impairments in brain disorders.
Why it matters
In human stem cell-derived neural cultures from children with Sanfilippo syndrome, a childhood dementia, the authors found hyperactive excitatory synapses and related gene dysregulation. The work is an in vitro model and supports drug discovery strategies targeting synaptic dysfunction, not a treatment or cure.
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The majority of individuals at 50% risk of carrying a pathogenic variant causing frontotemporal dementia (FTD) chooses not to undergo presymptomatic genetic testing.
Why it matters
This qualitative study of 28 Dutch people at risk of genetic frontotemporal dementia describes reasons for and against presymptomatic genetic testing, including wanting certainty versus fears about psychological impact, employment and insurance. It addresses decision-making about testing, not treating, curing or preventing the disease.
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The abnormal accumulation of hyperphosphorylated tau in neurofibrillary tangles is a hallmark of neurodegenerative diseases, such as Alzheimer's disease (AD) and frontotemporal dementia.
Why it matters
In the PS19 tau mouse model, spatial transcriptomics showed that glycolysis pathway genes, including Pgk1, were upregulated in the CA3 region at 2 months of age, before detectable tau tangles. The findings point to early metabolic dysregulation and glial activation in vulnerable brain regions, based on animal work.
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Epidemiological studies suggest that higher MedDiet adherence is associated with slower cognitive decline, reduced conversion from mild cognitive impairment to Alzheimer’s disease, and better motor and non-motor outcomes in Parkinson’s disease.
Why it matters
This review reports that Mediterranean diet adherence is linked to slower cognitive decline and that polyphenols such as resveratrol and oleuropein may contribute through antioxidant and other effects. Clinical studies are limited, and the authors call for long-term trials before any causal or treatment claim can be made.
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.
- Current Evidence for a Role of the Kynurenine Pathway of Tryptophan Metabolism in Multiple Sclerosis
- Similar deficits of central histaminergic system in patients with Down syndrome and Alzheimer disease
- Imaging phenotypes of major depressive disorder: genetic correlates
- Frontotemporal dementia associated CHCHD10V57E mutation aggravates tau pathology via disrupting the CHCHD10-Rab7A-TBC1D15 complex
- Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of Asp664
- Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury
- IRMA: Machine learning-based harmonization of $$^{18}$$F-FDG PET brain scans in multi-center studies
- Production and characterization of a monospecific antiserum (A128) to disaggregated Alzheimer paired helical filaments
- Tumor necrosis factor-alpha induces neurotoxicity via glutamate release from hemichannels of activated microglia in an autocrine manner
- Plasma Aβ and neurofilament light chain are associated with cognitive and physical function decline in non-dementia older adults