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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Our study is the first one showing that dietary supplements improve cognition and sleep in a mouse model of DS.
Why it matters
In a mouse model of Down syndrome, 4 weeks on a tryptophan-enriched diet improved short- and long-term memory, mood and sleep, though not social behaviour. Tryptophan is the building block of serotonin and melatonin, which help regulate mood and sleep. Because this was done in mice and the chemical changes behind it have not yet been measured, it points to a possible dietary approach worth studying rather than a proven benefit for people with Down syndrome or Alzheimer's.
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Tauopathies are characterized by aberrant tau structure and function, which is associated with neurodegenerative dementias, such as Alzheimer's disease, Pick's disease, and frontotemporal dementia, as well as the motor neuron disease amyotrophic lateral sclerosis.
Why it matters
This review explores how viruses and stress granules may interact with tau and contribute to tauopathies including Alzheimer's disease. It discusses possible insights for antiviral therapeutics but reports no treatment, cure or prevention.
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31/100
Neurodegenerative diseases are progressive disorders that damage and eventually kill neurons in the central nervous system (CNS).
Why it matters
This review examines curcumin-loaded nanostructures delivered through the nose to bypass the blood-brain barrier and increase curcumin's availability in the brain for neurodegenerative diseases. It is a review of delivery approaches, not a clinical trial, so no conclusions about treating or preventing Alzheimer's disease in patients can be drawn from it.
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The application of electrochemical sensors in medical testing is becoming increasingly widespread.
Why it matters
This study explores whether combining preoperative serum albumin with the mFI-5 frailty score can predict postoperative delirium in elderly hip fracture patients. It concerns prediction of a complication, not treatment, cure, or prevention of Alzheimer's disease.
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CWPs consist predominantly of two novel arrangements of type I Aβ filaments, and we have designated them as type Ic and type Id Aβ filaments.
Why it matters
This structural study describes two new arrangements of amyloid-beta filaments found in cotton wool plaques from people with Alzheimer's disease caused by specific PSEN1 mutations. It may help scientists understand how plaque structure varies and could inform future diagnostic and therapeutic strategies, but it does not test any treatment or prevention.
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Here we present our research design and preliminary results in ADAD mutation carriers and controls.
Why it matters
This report presents the design and preliminary results of a TMS study measuring cholinergic dysfunction in presymptomatic autosomal dominant Alzheimer's disease mutation carriers. It is early preliminary work aimed at understanding disease progression, not at treating or preventing Alzheimer's disease.
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We identified an interaction between TDP-43 and APOE through immunoprecipitation followed by proteomics in mice, verified in human brain by co- immunoprecipitation.
Why it matters
This study found that TDP-43 and APOE interact in mice, human brain and a cellular model of APOE4 overexpression, and that APOE post-translational modifications differ between AD patients without TDP-43 pathology and LATE patients with TDP-43 pathology. It describes a functional relationship between the two proteins but does not test or establish any treatment, cure or prevention.
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Primary cortical neurons with C9orf72 haploinsufficiency exhibit alterations in dendritic branching, indicating disrupted neuronal connectivity.
Why it matters
In cultured neurons with C9orf72 haploinsufficiency, the ALK inhibitor lorlatinib rescued dendritic complexity and improved resilience to glutamate-induced damage. These are cell-based findings related to C9orf72-FTD, not evidence of treating, curing or preventing Alzheimer's disease.
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Sundowning Syndrome (SS) is a clinically observed phenomenon, primarily associated with Alzheimer’s disease (AD), characterized by the exacerbation of neuropsychiatric symptoms during the late afternoon or evening, or in conditions of reduced ambient illumination.
Why it matters
This is a single case report of a patient who developed Sundowning Syndrome following hospitalization for a pneumothorax complicated by subcutaneous emphysema. As a case report, it cannot establish causation or provide generalizable evidence about treating, curing, or preventing Alzheimer's disease.
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When rs140926439 was absent, 0.10% of APOEε2/3 carriers had AD, while 0.43% of APOEε4 carriers or homozygotes had AD.
Why it matters
In UK Biobank data, a variant in the FN1 gene, rs140926439, was linked to lower Alzheimer's risk specifically in APOEε4 carriers, and the study suggests FN1 could be a target for future research. This is a genetic association finding, and the authors state that further research is needed to understand the mechanisms involved.
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Gene dysregulation in trisomy 21 can cause disorders of genes that are members of the heat-shock proteins (HSPs) family and contribute to the early onset of Alzheimer's disease (AD) in Down syndrome (DS).
Why it matters
This computer-based analysis of brain gene expression data suggests that certain heat-shock protein genes, especially the interaction between miR-155-5p and HSPA13, may be associated with Alzheimer's disease in Down syndrome. It is an in-silico study and provides no tested treatment, cure or prevention.
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Poly(ADP-ribosyl)ation (PARylation), a crucial post-translational modification, is catalyzed by ADP-ribosyltransferases (ARTs) and has significant implications in various cellular processes, including DNA damage response, cell signaling, and immune processes.
Why it matters
This review discusses how dysregulation of PAR signaling, either overactivation or suppression, may lead to neuronal dysfunction in several neurodegenerative diseases including Alzheimer. It does not report a treatment or cure, and the connections to disease onset are described as possible.
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It is associated with intracerebral hemorrhage (ICH), cognitive decline, and gait disturbance.
Why it matters
This case report describes cerebral amyloid angiopathy (CAA) in a patient carrying two copies of APOE ε2, a rare genotype linked to a higher risk of bleeding in CAA. Imaging showed recurrent bleeding on the brain surface, progressive cortical superficial siderosis, and a bleed within the brain and a surface bleed on opposite sides at the same time. The authors say it highlights how aggressive CAA can be in ε2/ε2 carriers, with repeated bleeding and iron build-up possibly injuring both blood vessels and brain tissue.
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Our research, conducted both in vivo and ex vivo, demonstrated a 50% decrease in pressure-induced constriction in the CADASIL ACT zone.
Why it matters
In tissue and animal experiments on CADASIL, a hereditary small vessel disease, pericytes in the affected zone showed KATP channel hyperactivity that modeling suggested reduces blood flow to layer IV of the cortex. This identifies a possible mechanism and target at the capillary level, but it is early laboratory work and does not show any treatment for Alzheimer's disease.
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This study shows promise for clarifying the relationship between the social exposome and ADRD brain pathology post‐mortem.
Why it matters
Among 740 brain bank donors, more years living in a more disadvantaged county was linked to a greater burden of vascular brain injury. This shows an association between life course social conditions and blood vessel changes in the brain but does not test any treatment or prevention.
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Oxidative stress in DS is associated with neurodevelopmental defects, neuronal dysfunction, and the onset of dementia re-sembling Alzheimer's disease.
Why it matters
In a mouse model of Down syndrome, ageing was linked to increased oxidative stress and liver fibrosis. This is animal research and does not test any treatment, cure or prevention for Alzheimer's disease in people.
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This individual had childhood-onset progressive motor impairment.
Why it matters
This case report describes one person with a GCH1 mutation and childhood-onset movement problems who improved greatly with levodopa-carbidopa and other therapy. It concerns a rare dopa-responsive movement disorder, not Alzheimer's disease, and reports a single individual.
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Transmissible encephalopathies (TSEs), such as Creutzfeldt-Jakob disease (CJD) and scrapie, are caused by infectious agents that provoke strain-specific patterns of disease.
Why it matters
This laboratory study identified host proteins bound to infectious particles in Creutzfeldt-Jakob disease after removing prion protein and other late-response proteins. It concerns prion disease, not Alzheimer's disease, and offers no treatment, cure, or prevention for Alzheimer's.
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This study offers evidence of functional and neuroprotective effects of two weeks treatment with a Ptychopetalum olacoides extract against Aβ peptide-induced neurotoxicity in mice.
Why it matters
In a mouse model of Alzheimer's-like dementia, 14 days of oral Marapuama extract prevented memory problems and reduced amyloid deposits and astrogliosis. This is early animal research only, so it does not show that Marapuama treats or prevents Alzheimer's disease in people.
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The 5' untranslated region (UTR) of the APP gene, encompassing 147 base pairs between the transcriptional (+1) and the translational start site, was examined for its role in APP expression.
Why it matters
This laboratory study identified a nuclear factor-binding domain in the 5' untranslated region of the amyloid precursor protein gene and found that eliminating factor binding reduced expression from the APP promoter. It is basic gene-regulation research and reports no treatment, cure or prevention for Alzheimer's disease.
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Down syndrome (DS) is a chromosomal abnormality (trisomy 21) associated with mental retardation and Alzheimer-like dementia, characteristic change of the individual's phenotype and premature ageing.
Why it matters
This study found signs of oxidative damage in blood from children with Down syndrome, along with lower coenzyme Q10 levels inside their cells. The authors link oxidative imbalance to the clinical features of Down syndrome, but no treatment or prevention was tested.
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Researchers since the 1990s have predominantly focused on the amyloid hypothesis and the formation of amyloid fibrils as the culprit behind AD when we began working on soluble Abeta (sAbeta).
Why it matters
This paper reports that N-terminal truncated peptides are the major components of soluble and insoluble amyloid beta in Alzheimer disease, that soluble amyloid beta species belong to the 42 form, and that soluble amyloid beta 42 is present in Down syndrome brains in prenatal and early postnatal development. It describes research findings about amyloid beta forms and reports no treatment or cure.
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Frontotemporal dementia regards a group of presenile progressive neurodegenerative form of dementias which includes Pick's disease, corticobasal degeneration, frontotemporal dementia with motor neuron disease, frontal lobe degeneration, dementia-parkinsonism-amyotrophy complex, familial non-specific dementia mapping to chromosome 3, non-Alzheimer degenerative dementia lacking distinctive histological features as well as a number other infrequent syndromes with dementia and focal neurological signs.
Why it matters
This study describes where metallothionein-I-II is found in the brains of people with frontotemporal dementia and its relationship to GFAP in astrocytes. It concerns frontotemporal dementia, not Alzheimer's disease, and does not test any treatment, cure, or prevention.
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31/100
Mutations in the human prion protein gene (PRNP) are responsible for hereditary diseases called transmissible spongiform encephalopathies (TSE) and a polymorphic site at codon 129 determines sensitivity to infectious forms of these maladies.
Why it matters
This study established conditions for detecting prion protein gene variants, including codon 129, using denaturing HPLC. It is a laboratory method for genetic screening and reports no treatment, cure or prevention for Alzheimer's disease.
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In persons with Down syndrome, soluble Abeta peptides, which result from the processing of the amyloid precursor protein, appear in the brain decades before the extracellular deposition of neuritic plaques.
Why it matters
This paper proposes that soluble Abeta peptides, especially Abeta1-42, form tight complexes with the alpha7 nicotinic acetylcholine receptor and may mediate progressive worsening of adaptive functions in Down syndrome. It is a hypothesis paper and does not show a treatment or cure.
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.
- SAMP8 mice as a neuropathological model of accelerated brain aging and dementia: Toshio Takeda's legacy and future directions
- Comparative In Vitro and In Vivo Quantifications of Pathologic Tau Deposits and Their Association with Neurodegeneration in Tauopathy Mouse Models
- Antioxidants in Down syndrome
- Local delivery of protease-resistant stromal cell derived factor-1 for stem cell recruitment after myocardial infarction
- CSF tau and β-amyloid predict cerebral synucleinopathy in autopsied Lewy body disorders
- Amyotrophic lateral sclerosis - frontotemporal spectrum disorder (ALS-FTSD): Revised diagnostic criteria
- Vascular and degenerative processes differentially affect regional interhemispheric connections in normal aging, mild cognitive impairment, and Alzheimer disease
- T cells specifically targeted to amyloid plaques enhance plaque clearance in a mouse model of Alzheimer's disease
- Therapeutic Effects of Transplanted Exosomes Containing miR-29b to a Rat Model of Alzheimer's Disease
- Age-related hearing loss accelerates cerebrospinal fluid tau levels and brain atrophy: a longitudinal study