Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 4,948 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Immunohistochemical staining with polyclonal antibodies to synthetic amyloid (residues 1-28 of A4) was performed on normal and Down syndrome brains from fetuses to adults.
Why it matters
This brain tissue study found that amyloid protein appears in developing brains and reappears in elderly brains, including in people with Down syndrome at an earlier age. The authors suggest this reappearance may relate to a regeneration process, but the study does not test any treatment.
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Studies of Alzheimer amyloid protein precursor mRNA expression in the human brain have provided compelling evidence for a neural origin of beta amyloid.
Why it matters
This early work found altered levels of amyloid precursor mRNA specifically in neurons at risk in Alzheimer's disease and Down syndrome, suggesting a neuronal source of beta amyloid. It raises the possibility that a shift toward the transcript containing the protease inhibitor domain may explain beta amyloid accumulation, but no treatment or prevention is tested here.
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Digital and palmar dermatoglyphics were examined in 29 men and 27 women with dementia of the Alzheimer type (DAT) and 112 age-, sex-, and racial group-matched controls.
Why it matters
This study found no dermatoglyphic differences between men with Alzheimer-type dementia and controls, and only limited differences in women, so it did not confirm earlier reports of such differences. It also failed to confirm a reported similarity between the dermatoglyphic pattern in Alzheimer's disease and that in Down syndrome, and it tests no treatment.
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31/100
In addition, we found sex-associated changes in the abundances of several proteins previously reported to be involved in tau pathology, such as Reelin, DARPP-32, Zyxin, Tbce, and Gng5, in JNPL3 mice.
Why it matters
In JNPL3 tauopathy mice, proteomics revealed altered membrane protein abundance in the prefrontal cortex, differing between males and females, including reduced levels of the drug efflux transporter ABCB1 in males. This is animal tissue analysis and identifies no treatment, cure or prevention.
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Neurodegenerative disorders (NDDs), primarily alzheimer, dementia, parkinson, and rare NDD disease, present an escalating global health crisis, currently affecting over 55 million older adults worldwide.
Why it matters
This is a plan for a scoping review that will map existing observational studies of GLP-1 receptor agonists in neurodegenerative disorders. It reports no new results and therefore cannot say whether these drugs treat or prevent Alzheimer's disease.
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Down syndrome (DS), caused by trisomy of chromosome 21, is characterized by early-onset oxidative stress, impaired neuronal development, and an increased risk of Alzheimer's disease (AD)-like neuropathology.
Why it matters
This review proposes that dysregulation of the BACH1/HO-1 axis links Down syndrome to Alzheimer-like neurodegeneration and discusses BACH1 inhibitors and NRF2 activators as emerging strategies. These are proposed approaches only, with no tested treatment or cure in people.
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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.
From across this topic
10 of the 4,930 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