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 results show that genotype, AOF, and sex contributed to AD-like pathology.
Why it matters
In female 5xFAD mice, amyloid-beta aggregation increased around perimenopause along with some glial activation in specific hippocampal regions, but cognitive function was not affected. This is early animal research supporting the idea that perimenopause may be a period of susceptibility, not proof of a treatment or prevention.
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Alzheimer's disease is the leading cause of dementia worldwide.
Why it matters
This review proposes that the plant compound quercetin may reduce neuroinflammation by modulating the P2X7 receptor. It presents a hypothesis based on existing evidence rather than testing quercetin as a treatment in patients.
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35/100
Neurodegeneration in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) results from both gain of toxicity and loss of normal function of the RNA-binding protein TDP-43, but their mechanistic connection remains unclear.
Why it matters
Using a cell-based seeding platform, this study showed that TDP-43 aggregates can be taken up by human neuron-like cells, recruit normal TDP-43 and cause loss of function. These are laboratory findings about how pathology may spread, not a treatment or prevention for patients.
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Mutations in the Integral membrane protein 2B (ITM2B) gene are linked to the development of familial British and Danish dementias, two relatively early-onset dementia disorders known also to be associated with Tau neurofibrillary tangles (NFTs).
Why it matters
This study used a small number of brain samples (n = 4 per disease state) and found that ITM2B co-localized frequently with tau pathology but far less with TDP-43 pathology. This suggests ITM2B has little if any role in the relationship between tau and TDP-43, so it is not a promising treatment target for that interaction.
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The current study provides opportunities for safer approaches that using compounds derived from plants and links it to nanotechnology, could be used in the pharmaceutical industry to treat Alzheimer’s disease.
Why it matters
In mice with lipopolysaccharide-induced Alzheimer-like changes, a nanoemulsion of Origanum majorana essential oil improved cognitive function and lowered AChE, TLR4 and GFAP levels compared with untreated mice. This is an animal study only, so it does not show any benefit for people with Alzheimer's disease.
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35/100
The enzyme pair PINK1 and PRKN together orchestrates a cytoprotective mitophagy pathway that selectively tags damaged mitochondria with phospho-serine 65 ubiquitin (pS65-Ub) and directs them for autophagic-lysosomal degradation (mitophagy).
Why it matters
In autopsy brain tissue from people with MAPT-associated frontotemporal dementia with parkinsonism, a marker of mitophagy called pS65-Ub accumulated strongly in P301L cases but only weakly in N279K cases, with different patterns across hippocampal regions. This describes disease processes in brain tissue and does not test a treatment.
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The data suggest that TNFSF10 system-targeted treatment effectively restrain overshooting central and peripheral inflammation by rebalancing the overall immune response, mitigating the progression of AD pathology.
Why it matters
In a mouse model of Alzheimer's disease, blocking the immune signal TNFSF10 for three months shifted microglia and spleen macrophages toward a less inflammatory state and reduced certain inflammatory immune cells. These are animal findings, so it is not yet known whether this approach would help people.
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Chronic cerebral hypoperfusion induced by permanent unilateral common carotid artery occlusion in mice was recently found to induce an age-dependent formation of insoluble cytoplasmic TDP-43 aggregates reminiscent of pathological changes found in human vascular dementia.
Why it matters
In a mouse model of chronic cerebral hypoperfusion, virus-mediated delivery of a single-chain antibody against TDP-43 reduced cytoplasmic TDP-43 aggregates and prevented cognitive impairment and motor deficits. These results suggest TDP-43 should be considered a therapeutic target, but the work is in mice and not yet tested in humans.
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35/100
This chapter discusses the dependency of basal forebrain cholinergic neurons (BFCNs) on endogenous nerve growth factor (NGF) for the structural and physiologic maintenance of the neuronal cell somata, axonal projections, and terminal synapses.
Why it matters
This chapter describes how basal forebrain cholinergic neurons depend on nerve growth factor and how this pathway is dysregulated in Alzheimer's disease and Down syndrome. It is a mechanistic review and does not report a tested treatment, cure or prevention.
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< 0.0036), the MCRS group exhibited significantly worse performance on word list memory, word list recall, and MMSE-KC compared to the MCI group without slow gait.
Why it matters
Among people with mild cognitive impairment, those with motoric cognitive risk syndrome had worse memory and MMSE-KC scores and greater white matter hyperintensity burden than those without slow gait. This describes a more severe clinical subgroup but does not test any treatment, cure, or prevention.
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Down syndrome (DS) is the most common genetic cause of intellectual impairment, characterised by an extra copy of chromosome 21.
Why it matters
This paper describes how altered brain insulin and IGF-1 signaling, including the PI3K-Akt/mTOR axis, may contribute to early Alzheimer-like pathology in Down syndrome. It proposes this axis as a potential therapeutic target, but no treatment or trial in people is reported.
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Previous research has found that living in a disadvantaged neighborhood is associated with poor health outcomes.
Why it matters
In brain tissue from 159 donors, one DNA methylation site was linked to neighborhood deprivation, and this link was mainly seen in people carrying at least one APOE ε4 allele. This points to a possible biological pathway related to immune response, but it is not a treatment or prevention finding.
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The Aβ hypothesis has long been central to Alzheimer's disease (AD) theory, with a recent surge in attention following drug approvals targeting Aβ plaque clearance.
Why it matters
This laboratory study found that co-aggregates of Aβ42 and human islet amyloid polypeptide worsened neurotoxicity and Alzheimer-like pathology at the cellular level. It is early cell-based work and does not show any treatment, cure or prevention for people.
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Prohibitin 1 (PHB1) and prohibitin 2 (PHB2) are proteins that are nearly ubiquitously expressed.
Why it matters
This review describes prohibitin 1 and 2 as proteins involved in many brain functions and reports increasing evidence that they are involved in numerous brain disorders including Alzheimer's disease and Down syndrome. It states plainly that no therapy targeting prohibitins is available for any of these diseases.
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Genome-wide deregulation contributes to mitochondrial dysfunction and impairment in oxidative phosphorylation (OXPHOS) mechanism resulting in oxidative stress, increased production of reactive oxygen species (ROS) and cell death in individuals with Down syndrome (DS).
Why it matters
This review discusses how mitochondrial dysfunction and oxidative stress in Down syndrome may contribute to cognitive problems and early Alzheimer's disease, and mentions natural compounds such as polyphenols, antioxidants and flavonoids as showing promising results. It reports no confirmed treatment, cure or prevention for Alzheimer's disease.
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We believe that the amyloid-PET scans, perceived as showing decreasing amyloid deposits, are an expression of increased cerebral cell death due to aducanumab treatment, so that with time one should instead expect a worsening and not an improvement in the treated patients' condition.
Why it matters
The authors argue that the FDA's accelerated approval of aducanumab was based exclusively on a perceived dose-dependent reduction in brain amyloid deposits rather than a proven clinical effect. They believe the amyloid-PET scans may reflect increased cerebral cell death, so they expect worsening rather than improvement in treated patients.
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An enriched environment is effective in stimulating learning and memory in animal models as well as in humans.
Why it matters
In this 6-week randomized intervention in healthy older adults, curiosity-based interventions increased an everyday functioning score but did not change serum BDNF levels. It reports no effect on that biomarker and does not show that the intervention treats, cures or prevents Alzheimer's disease.
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These findings suggest that neurotrophic impairment during early development can be one of the etiopathogenic factors of AD and that the neurotrophic peptide mimetic is a potential early prevention strategy for this disease.
Why it matters
In 3xTg-AD mice, prenatal to early postnatal treatment with the neurotrophic compound P021 rescued cognitive deficits at 4 months and reduced tau and amyloid plaque pathology later. This is an animal study and does not show that this approach treats, cures or prevents Alzheimer's disease in people.
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Prenatal exposure to low doses of LPS caused AD-related features including behavioral and neuropathological changes from midlife to senectitude.
Why it matters
Mice exposed to lipopolysaccharide during late embryogenesis developed Alzheimer-like behavioral and neuropathological changes from 12 months onward, including increased Aβ42, p-tau and GFAP. This is animal research suggesting a possible link between early infection and later Alzheimer-like changes, not a treatment or cure.
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Alzheimer disease has been well associated with mitochondrial dysfunctions.
Why it matters
In a streptozotocin-induced rat model of sporadic dementia of Alzheimer's type, prolonged treatment with Trans-ferulic acid rescued memory and learning problems, showed antioxidant effects, preserved hippocampal pyramidal cell morphology, and mitigated bioenergetics loss and changes in mitochondrial dynamics. The authors conclude ferulic acid may mitigate mitochondrial dysfunction in Alzheimer's disease on prolonged dietary supplementation, but these are animal findings and do not establish a treatment or cure for people.
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Epidemiological studies have reported that highly fluoridated drinking water may significantly decrease the Intelligence Quotient (IQ) of exposed children.
Why it matters
In rats sub-chronically exposed to fluoride in drinking water, fluoride activated microglia, released pro-inflammatory cytokines and influenced synaptic neuron plasticity in the hippocampus. This is an animal study of fluoride exposure, so it does not provide evidence about treating, curing or preventing Alzheimer's disease.
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An important worldwide health problem as the result of current lifestyle is metabolic syndrome (MS).
Why it matters
In rats, combining metabolic syndrome with an injection of amyloid beta 1-42 worsened memory and increased markers of oxidative stress and inflammation. This is animal research and does not show any treatment, cure, or prevention for people.
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For the association analysis of whole-genome sequencing (WGS) studies, we propose an efficient and fast spatial-clustering algorithm.
Why it matters
This paper proposes a statistical method for grouping genetic variants into regions when analyzing whole-genome sequencing data. It is a methods paper and reports no findings about treating, curing, or preventing Alzheimer's disease.
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Currently, several immunotherapies and BACE (Beta Site APP Cleaving Enzyme) inhibitor approaches are being tested in the clinic for the treatment of Alzheimer's disease.
Why it matters
This study used aged APP transgenic mice to investigate whether long-term BACE inhibitor therapy worsens microhemorrhages, a safety concern because such bleeds are already present in most Alzheimer patients. The findings come from animal research, not from people.
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Alzheimer's disease (AD) is the most common cause of dementia in the elderly population.
Why it matters
In 3-month-old triple transgenic Alzheimer's disease mice, increased protein carbonylation was found in the hippocampus, supporting the view that oxidative stress is an early event in Alzheimer's disease progression. This is early animal research and does not establish any treatment, cure, or prevention for people.
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.
- A role for docosahexaenoic acid-derived neuroprotectin D1 in neural cell survival and Alzheimer disease
- [Biochemical alterations in patients with Down syndrome]
- Induced dimerization of the amyloid precursor protein leads to decreased amyloid-beta protein production
- Hippocampal and amygdalar volumes in dissociative identity disorder
- Human neural stem cell-derived extracellular vesicles mitigate hallmarks of Alzheimer's disease
- Human ETS2 gene on chromosome 21 is not rearranged in Alzheimer disease
- Activation of Toll-like receptor 2 on microglia promotes cell uptake of Alzheimer disease-associated amyloid beta peptide
- Yogic meditation reverses NF-κB and IRF-related transcriptome dynamics in leukocytes of family dementia caregivers in a randomized controlled trial
- S-adenosylmethionine reduces the progress of the Alzheimer-like features induced by B-vitamin deficiency in mice
- Biology of posttraumatic stress disorder