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 degeneration of neurones in Parkinson's disease (PD) may involve oxidative stress.
Why it matters
In post-mortem brain tissue, protein carbonyl levels were increased in Parkinson's disease but not in incidental Lewy body disease, and the authors suggest this may relate to L-DOPA treatment rather than to the disease process itself. This concerns Parkinson's disease and oxidative damage, not Alzheimer's treatment, cure or prevention.
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Among the 30 boxers, 11 were found to be normal (CBI score=0), 12 showed mild deficits (CBI score=1-2), 4 were moderately impaired (CBI score=3-4), and 3 showed signs of severe impairment (CBI score > 4).
Why it matters
In this study of 30 professional boxers, high-exposure boxers had significantly higher scores on a chronic brain injury scale, and APOE genotype was examined in relation to these measures. It is a small study and does not report a treatment, cure, or prevention for Alzheimer's disease.
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The community-based Rotterdam Study, the Netherlands.
Why it matters
This study examined whether high dietary intake of antioxidants is associated with the risk of Parkinson disease in a community-based population. It is about Parkinson disease, not Alzheimer's disease, and does not test any treatment, cure, or prevention for Alzheimer's.
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Proteolytic processing of amyloid precursor protein (APP) through an endosomal/lysosomal pathway generates carboxy-terminal polypeptides that contain an intact beta-amyloid domain.
Why it matters
In mice engineered to make the last 104 amino acids of the amyloid precursor protein (APP), the study reports that with ageing they developed "extracellular beta-amyloid immunoreactivity, increased gliosis and microglial reactivity, as well as cell loss in the CA1 region of the hippocampus." It supports the idea that "changes in APP metabolism may be important" in Alzheimer's disease. This is animal research with no human data and no treatment.
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The PDAPP transgenic mouse, which overexpresses human amyloid precursor protein (APP717V-->F), has been shown to develop much of the pathology associated with Alzheimer disease.
Why it matters
In PDAPP mice engineered to overproduce a mutant human amyloid precursor protein (APP), this 1997 study measured APP and amyloid-beta (Aβ) in brain regions between 4 and 18 months of age. APP levels stayed 'nearly constant', while Aβ rose sharply where plaques formed: in the hippocampus it increased 17-fold from 4 to 8 months and over 500-fold by 18 months. Because some plaque-free regions made more APP than some plaque-prone ones, the authors suggest 'regionally specific factors also seem important'; this was a mouse study and tested no treatment.
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Cortical-basal ganglionic degeneration classically presents predominantly as a motor disorder with a unique constellation of histological alterations characterized by the presence of neuronal loss and gliosis in a selective distribution, swollen achromasic neurons, and extensive deposition of abnormal tau in neurons and glia.
Why it matters
This report describes 3 patients with cortical-basal ganglionic degeneration who presented with cognitive changes or language disturbance, and concludes the condition should be considered in the differential diagnosis of language disturbances and dementia. It concerns diagnosis of a different neurodegenerative condition, not Alzheimer's treatment, cure or prevention.
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The 39- to 43-amino acid amyloid beta-protein (A beta), which is progressively deposited in cerebral plaques and blood vessels in Alzheimer disease (AD), is secreted by cultured human cells during normal metabolism.
Why it matters
Skin cells from people carrying the Swedish familial Alzheimer's disease mutation produced more amyloid-beta protein than cells from unaffected relatives or spouses. This laboratory finding supports the idea that this mutation increases amyloid-beta production, but it does not test a treatment or prevention.
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Antibodies to ubiquitin have been used to search for evidence of abnormal protein degradation in amyotrophic lateral sclerosis--motor neuron disease (ALS).
Why it matters
This study found ubiquitin-immunoreactive inclusions in the lower motor neurons of all 31 people with amyotrophic lateral sclerosis, a characteristic feature of that disease. It is about ALS pathology, not about treating, curing, or preventing Alzheimer's disease.
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48/100
Interleukin 1, an immune response-generated cytokine that stimulates astrocyte proliferation and reactivity (astrogliosis), was present in up to 30 times as many glial cells in tissue sections of brain from patients with Down syndrome and Alzheimer disease compared with age-matched control subjects.
Why it matters
This tissue study found interleukin 1 in up to 30 times as many glial cells in brain tissue from people with Down syndrome and Alzheimer disease compared with controls, and elevated levels of S-100 and glial fibrillary acidic protein. It is a descriptive finding about inflammation and reports no treatment, cure or prevention.
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The intraneuronal accumulation of paired helical filaments in the form of neurofibrillary tangles is one hallmark of the brain pathology in Alzheimer's disease.
Why it matters
This study used quantitative immunocytochemistry and a morphological classification of neurofibrillary tangles to show that accumulation of abnormally phosphorylated tau precedes the formation of the tangles in Alzheimer's disease. It describes a step in disease pathology and reports no treatment, cure or prevention.
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We studied forty patients with CT-proven thalamic infarcts without involvement of the superficial territory of the posterior cerebral artery.
Why it matters
This study of 40 patients with thalamic infarcts describes clinical syndromes, causes and outcomes, including thalamic dementia as a cause of late disability. It concerns strokes in a specific brain region and does not address treating, curing or preventing Alzheimer's disease.
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Individuals with Down syndrome (DS) are at high risk for Alzheimer's disease (AD), yet accessible tools for routine clinical screening of AD in individuals with DS remain limited.
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47/100
These findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer’s disease.
Why it matters
This study found no significant difference in a blood marker of Alzheimer's tau pathology between young adults with Down syndrome regression disorder, those with Down syndrome without regression, and controls. The results suggest that this regression disorder is not associated with an Alzheimer's-like tau pattern.
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Dementia in individuals with Down syndrome (DS) is the leading cause of early-onset cognitive decline occurring before the age of 50.
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Neurodegenerative diseases, including Alzheimer's Disease (AD), Parkinson's Disease (PD), Lewy Body Disease (LBD), and related dementias, represent a global health challenge, particularly in aging populations.
Why it matters
This review synthesizes evidence that neurodegenerative proteins including amyloid-β, tau, α-synuclein, TDP-43, and FUS share characteristics of intrinsically disordered proteins, which may explain mixed pathology and cross-seeding. It highlights the need for integrative, systems-level approaches to identify novel targets, but no specific treatment is tested or proposed.
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A total of 30 variants were overrepresented in four pathways: presenilin/Alzheimer disease, cadherin/WNT signaling, gonadotropin-releasing hormone receptor, and transforming growth factor-β (TGF-β) signaling.
Why it matters
This study is about colorectal cancer risk and found an interaction between TGF-β pathway variants and red meat intake; an Alzheimer disease pathway appeared only among the pathways analyzed. It reports no treatment, cure, or prevention findings for Alzheimer disease.
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A case-control GWAS was performed in the UK Biobank to identify genetic variants associated with postoperative delirium, adjusted for age, sex, genetic chip, and the first 10 principal components.
Why it matters
This genome-wide association study found shared genetic architecture and risk between postoperative delirium and Alzheimer's disease, with the APOE ε4 isoform showing a dose-response effect on delirium risk. The findings point to a genetic link between the two conditions but do not test any treatment, cure or prevention.
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Alzheimer's disease (AD) and vascular dementia (VaD) exhibit distinct neuropathological hallmarks, with AD defined by cortical amyloid plaques and neurofibrillary tangles, while VaD arises primarily from cerebrovascular disease (CeVD).
Why it matters
In this study of 531 participants, serum ASC levels were increased in vascular cognitive impairment subgroups compared to controls, and this association appeared largely explained by the severity of white matter hyperintensities. The authors say elevated serum ASC may reflect inflammasome activation in vascular cognitive impairment, but the study does not test any treatment, cure, or prevention.
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Our study reveals that PS in DLB is associated with specific deficits in attention and visuospatial/executive function, alongside more severe neuropsychiatric symptoms.
Why it matters
In this study of 218 patients with dementia with Lewy bodies, those with Pisa syndrome had significantly worse attention and visuospatial/executive abilities and more neuropsychiatric symptoms. They also had higher caregiver burden scores.
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Lewy body dementia is the second most common form of neurodegenerative dementia, following Alzheimer's disease.
Why it matters
This review describes the neuropathology of Lewy body dementia, including Lewy-related pathology, α-synuclein oligomers, and comorbid conditions such as Alzheimer's disease neuropathologic change. It is a description of disease mechanisms and does not report any treatment, cure, or prevention.
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: Aβ-β-amyloid; AD-Alzheimer disease; APMS-affinity purification mass spectrometry; APOE-apolipoprotein E; APP-amyloid beta precursor protein; BafA1-bafilomycin A1; CMA-chaperone-mediated autophagy; COP-coatomer; ER-endoplasmic reticulum; ERAD-endoplasmic reticulum-associated degradation; ERGIC-endoplasmic reticulum-Golgi intermediate compartment; FCCP-carbonyl cyanide p-trifluoromethoxyphenylhydrazone; GABA-gamma-aminobutyric acid; GFP-green fluorescent protein; GPI-glycerophosphoinositol; GPN-glycyl-L-phenylalanine 2-naphthylamide; HA-hemagglutinin protein tag; iPSC-induced pluripotent stem cells; LAMP1-lysosomal associated membrane protein 1; LGALS3BP-galectin 3 binding protein; LysoIP-lysosomal immunoprecipitation; MAPT-microtubule associated protein tau; MR-CTSB-magic red cathepsin B; MS-mass spectrometry; NFT-neurofibrillary tangles; PCA-principal component analysis; PLA-proximity ligation assay; PSEN1-presenilin 1; PSEN2-presenilin 2; p-MAPT/Tau-phospho-MAPT/tau; ROS-reactive oxygen species; RT-qPCR-reverse transcriptase quantitative polymerase chain reaction; SEM-standard error of the mean; siRNA-short interfering RNA; SRCR-scavenger receptor cysteine-rich domain; TMED-transmembrane p24 trafficking protein; TMEM192-transmembrane protein 192.
Why it matters
This study used lysosomal proteomics to investigate how the APOE4 form of apolipoprotein E may cause lysosomal dysfunction in neurons. It is a laboratory study and does not report a treatment or prevention for Alzheimer disease.
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GLP-1RA use was associated with lower risk of dementia (HR 0.80, 95% CI 0.71–0.91) and Alzheimer’s disease (HR 0.76, 95% CI 0.59–0.98) compared to DPP4is.
Why it matters
In this real-world study of people with diabetes and advanced chronic kidney disease, those taking GLP-1 receptor agonists had a lower risk of dementia and Alzheimer's disease diagnoses than those taking DPP4 inhibitors. No significant differences were found for other conditions such as vascular dementia or Parkinson's disease.
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Immune mechanisms contribute to the neuropathology of Alzheimer's disease (AD) but the role of adaptive immune cells is unclear.
Why it matters
In a mouse model, removing certain brain CD8 T cells improved cognition and reduced neuropathology, and a signaling pathway involving granzyme K and PAR-1 was identified. This is early animal and cell work pointing to a possible target, not a treatment for patients.
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TANK-Binding Kinase 1 (TBK1) is involved in autophagy and immune signaling.
Why it matters
In mice, deleting Tbk1 from microglia produced an aged-like, pro-inflammatory microglial signature and caused social recognition deficits resembling frontotemporal dementia, without affecting motor neuron damage. This is animal research on ALS/FTD mechanisms and does not address treating or preventing Alzheimer's disease.
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Cerebral small vessel disease (cSVD) is associated with vascular cognitive impairment, dementia, and stroke.
Why it matters
In this cross-sectional study, patients with cerebral small vessel disease had higher leakage tissue volume and lower blood plasma volume within white matter hyperintensities compared to controls, but the leakage rate itself did not differ in any region. The findings describe a spatial pattern of blood-brain barrier leakage that may be caused by local reductions in microvascular blood flow or vessel surface area, but they do not test any treatment, cure, or prevention.
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.
- Cognitive and Biomarker Signatures of Late-Onset Temporal Lobe Epilepsy: Toward Non-Alzheimer Neurodegenerative Mechanisms
- Amygdala parcellation reveals unique subregions of atrophy in FTLD‐tauopathies
- Cutting Edge: Inhibition of TLR and FcR Responses in Macrophages by Triggering Receptor Expressed on Myeloid Cells (TREM)-2 and DAP12
- Fluvoxamine maleate alleviates amyloid-beta load and neuroinflammation in 5XFAD mice to ameliorate Alzheimer disease pathology
- Sequential distribution of pTDP-43 pathology in behavioral variant frontotemporal dementia (bvFTD)
- Differentially expressed genes in Alzheimer's disease highlighting the roles of microglia genes including OLR1 and astrocyte gene CDK2AP1
- Clonal expansion of cytotoxic CD8⁺ T cells in lecanemab-associated ARIA
- Microbiome–metabolome dynamics associated with impaired glucose control and responses to lifestyle changes
- Transcriptomic analysis from 3D cultures of Presilinin‐1 G206A carriers reveals genetic expression differences associated with age‐of‐onset variability
- Sequential proteolytic processing of the triggering receptor expressed on myeloid cells-2 (TREM2) protein by ectodomain shedding and γ-secretase-dependent intramembranous cleavage