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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Stress granules and P bodies are conserved cytoplasmic aggregates of nontranslating messenger ribonucleoprotein complexes (mRNPs) implicated in the regulation of mRNA translation and decay and are related to RNP granules in embryos, neurons, and pathological inclusions in some degenerative diseases.
Why it matters
Using baker's yeast and mammalian cells, this study found that stress granules are cleared by autophagy and that this clearance is reduced by mutations in VCP, which predispose humans to ALS and frontotemporal lobar degeneration. It suggests that autophagic clearance of these granules may be important in reducing pathology, but this is laboratory research and not a treatment tested in patients.
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Recent evidence suggests that rare genetic variants within the TREM2 gene are associated with increased risk of Alzheimer's disease.
Why it matters
In one Colombian family from Antioquia, whose parents were related and in which behavioural-variant frontotemporal lobar degeneration ran as a recessive trait, this 2013 study reports that TREM2 gene variants are associated with that condition and with Alzheimer's disease. The stored abstract stops before its results, so it does not say which variant was found, how many people carried it, or how the Alzheimer's link was tested. The idea that losing TREM2 function harms the brain's clean-up of dead cells is stated as background, not as something this study showed.
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Tauopathies, including Alzheimer's disease (AD) and frontotemporal lobar degeneration with tau pathologies, are neurodegenerative diseases characterized by neurofibrillary tangles (NFTs) comprising filamentous tau protein.
Why it matters
In mice engineered to carry a mutant human tau gene (PS19, P301S), injecting lab-made tau fibrils into the brain "resulted in rapid induction of NFT-like inclusions that propagated from injected sites to connected brain regions," with a different spreading pattern depending on whether the hippocampus or striatum was injected. The authors report these induced tangles "more closely resembled AD NFTs" than the tau clumps the mice develop on their own with age. This is an animal model showing that tau pathology can be seeded and spread along brain connections; it is not evidence about how the disease starts in people, and it tests no treatment.
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The Monotherapy Switzerland/Thailand study (MOST) trial compared monotherapy with ritonavir-boosted lopinavir with continued therapy.
Why it matters
This study looked at cerebrospinal fluid markers, including the astrocytic marker S100B, in HIV-infected patients taking lopinavir/ritonavir monotherapy, a trial stopped early because of virological failure. It concerns HIV brain markers, not Alzheimer's disease, so it has no direct implications for treating, curing or preventing Alzheimer's.
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The C9orf72 expansion is a common cause of ALS and FTLD, but not of AD or PD.
Why it matters
The C9orf72 repeat expansion was found in ALS and frontotemporal lobar degeneration but not in Alzheimer disease cases or controls. This argues the expansion is not a cause of Alzheimer disease and does not test any treatment.
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The accumulation of Tau into aggregates is associated with key pathological events in frontotemporal lobe degeneration (FTD-Tau) and Alzheimer disease (AD).
Why it matters
In lab experiments, neurons took up small misfolded tau clumps and short fibrils, but not single tau molecules or long fibrils, and moved them along their axons in both directions. Whether uptake happened depended on the clumps' size and shape, and the clumps sat alongside a marker of bulk endocytosis. The authors report that the clumps "can enhance tauopathy in vivo". No human patients were studied and no treatment was tested.
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The long-chain ω-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are potential candidates for interventions to delay Alzheimer disease (AD), but evidence from clinical studies is mixed.
Why it matters
In older community dwellers, higher plasma EPA but not DHA was linked to less gray matter atrophy in the right hippocampal/parahippocampal area and right amygdala over four years. This is an observational finding and does not show that taking these fatty acids prevents Alzheimer's disease.
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Stepwise decreases in WM integrity as measured by both DTI and FLAIR were independently associated with stepwise increases in WMH risk, emphasizing that these modalities may provide complementary information for understanding the time course of aging-associated WM degeneration.
Why it matters
In 119 participants including healthy elders and people with Alzheimer disease or mild cognitive impairment, lower baseline fractional anisotropy and higher FLAIR signal independently predicted which normal-appearing white matter regions would later become white matter hyperintensities. This is a longitudinal imaging study of white matter degeneration, not a test of any treatment, cure, or prevention.
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We have used a translational convergent functional genomics (CFG) approach to identify and prioritize genes involved in schizophrenia, by gene-level integration of genome-wide association study data with other genetic and gene expression studies in humans and animal models.
Why it matters
This study used a convergent functional genomics approach to identify and prioritize genes involved in schizophrenia and to generate a genetic risk prediction score. It concerns schizophrenia, not Alzheimer disease, and provides no information about treating, curing, or preventing Alzheimer disease.
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Accumulations of insoluble deposits of amyloid β-peptide are major pathological hallmarks of Alzheimer disease.
Why it matters
This chapter describes how amyloid-beta is produced from amyloid precursor protein by sequential cleavage by beta- and gamma-secretases, while alpha-secretase prevents its generation. It explains the basic biology of amyloid-beta production but does not report a treatment or cure.
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52/100
Prions are self-templating protein conformers that are naturally transmitted between individuals and promote phenotypic change.
Why it matters
This review argues that many RNA-binding proteins with prion-like domains, including FUS and TDP-43, are emerging in the genetics and pathology of neurodegenerative diseases. It is a hypothesis-generating review with no treatment tested.
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Increased (11)C-DED binding throughout the brain of the MCI (11)C-PIB+ patients potentially suggests that astrocytosis is an early phenomenon in AD development.
Why it matters
Using a PET tracer for astrocytes, increased binding was found in the frontal and parietal cortices of MCI patients, suggesting astrocytosis may be an early phenomenon in Alzheimer disease development. This was a small study of 8 MCI, 7 Alzheimer, and 14 control participants.
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Disinhibition is a common behavioural symptom in frontotemporal dementia but its neural correlates are still debated.
Why it matters
In this small study of 14 people with behavioral variant frontotemporal dementia and 15 with Alzheimer's disease, disinhibition was linked to atrophy in specific brain regions including the orbitofrontal cortex. This helps understand the brain changes behind disinhibition but does not offer a treatment or cure.
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52/100
To identify rare causal variants in late-onset Parkinson disease (PD), we investigated an Austrian family with 16 affected individuals by exome sequencing.
Why it matters
This study identified a VPS35 mutation causing late-onset Parkinson's disease in an Austrian family and additional families, with a mean age of onset of 53 years. It concerns Parkinson's disease genetics, not Alzheimer's disease, so it does not directly inform Alzheimer's treatment, cure or prevention.
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The hippocampal formation plays an important role in cognition, spatial navigation, learning, and memory.
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TDP-43 and FUS are RNA-binding proteins that form cytoplasmic inclusions in some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD).
Why it matters
Using a yeast model and purified FUS, this study found that FUS aggregation and toxicity require a prion-like domain and RGG domain determinants, and that ALS-linked FUS mutations do not promote aggregation. It suggests TDP-43 and FUS cause disease by distinct mechanisms, which may affect treatment design, but it is laboratory work.
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Late-onset Alzheimer's disease (LOAD) is the most common form of dementia in the elderly.
Why it matters
This family-based genome-wide association study replicated BIN1 and CLU and nominated CUGBP2 in interaction with APOE for late-onset Alzheimer's disease. It is genetic research into disease risk and does not provide a treatment, cure, or prevention.
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52/100
Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) are characterized by cytoplasmic protein aggregates in the brain and spinal cord that include TAR-DNA binding protein 43 (TDP-43).
Why it matters
Mice expressing human TDP-43 with a defective nuclear localization signal showed neuron loss and motor symptoms, and neurodegeneration was accompanied by loss of the normal mouse TDP-43 rather than by cytoplasmic inclusions. This is animal research suggesting that loss of normal TDP-43 function may matter, but no treatment was tested in people.
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Adverse childhood events are related to continued vulnerability among older adults, enhancing the impact of chronic stressors.
Why it matters
In 132 older adults, childhood adversity was linked to higher inflammation markers and shorter telomeres, and abuse effects on one marker were larger in dementia caregivers. This is about stress biology in caregivers and does not test any treatment, cure or prevention for Alzheimer's disease.
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52/100
Prospective studies have shown that although the beneficial effects of this procedure are maintained at 5 years, axial motor features and cognitive decline may occur in the long term after the implants.
Why it matters
This study followed Parkinson's disease patients eight years after subthalamic implants and found that motor improvement was only partly retained, with worsening speech and postural stability and a slight decline in some cognitive tasks. It concerns Parkinson's disease and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Our results suggest that decreased hippocampal tail and hippocampal head volumes could be trait changes, whereas hippocampal body changes may be dependent on treatment.
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Autophagy is an intracellular degradation pathway that functions in protein and organelle turnover in response to starvation and cellular stress.
Why it matters
In laboratory work, activating autophagy reduced levels of amyloid precursor protein and its breakdown products, suggesting a possible way to lower these proteins. This is early mechanistic research and does not show that boosting autophagy helps patients or changes the course of Alzheimer's disease.
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Neuronal cytoplasmic and intranuclear aggregates of RNA-binding protein TDP-43 are a hallmark feature of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD).
Why it matters
In mice, making wild-type human TDP-43 caused motor neuron degeneration and paralysis along with TDP-43 aggregates like those in ALS and FTLD patients. This is animal work only, and it suggests that a toxic gain of function by TDP-43 fragments may harm neurons, but no treatment is tested here.
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52/100
Progranulin (PGRN) is a widely expressed protein involved in diverse biological processes.
Why it matters
Mice lacking progranulin showed exaggerated inflammation, impaired host defense and, with age, more microglial and astrocytic activation plus accumulation of phosphorylated TDP-43 in neurons. This suggests frontotemporal dementia from progranulin insufficiency may involve reduced neurotrophic support and dysregulated inflammation, but it is an animal study and reports no treatment or cure.
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Cytoplasmic inclusions containing alpha-synuclein (alpha-Syn) fibrils, referred to as Lewy bodies (LBs), are the signature neuropathological hallmarks of Parkinson's disease (PD).
Why it matters
In cultured cells overexpressing alpha-synuclein, introducing exogenous alpha-synuclein fibrils triggered aggregation into insoluble, hyperphosphorylated and ubiquitinated species resembling Lewy bodies. This is a cell model supporting the concept that small quantities of fibrils can seed aggregation, not a treatment or prevention study.
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.
- Dendritic spinopathy in transgenic mice expressing ALS/dementia-linked mutant UBQLN2
- Resveratrol mediates mechanical allodynia through modulating inflammatory response via the TREM2-autophagy axis in SNI rat model
- Proteomic signatures and aberrations of mouse embryonic stem cells containing a single human chromosome 21 in neuronal differentiation: an in vitro model of Down syndrome
- Human Induced Pluripotent Stem Cell-Derived Microglia-Like Cells Harboring TREM2 Missense Mutations Show Specific Deficits in Phagocytosis
- RAC1 inhibition targets amyloid precursor protein processing by gamma-secretase and decreases Abeta production in vitro and in vivo
- Assessing Co‐Localization of ITM2B With Alzheimer's Disease and Limbic‐Predominant Age‐Related TDP ‐43 Encephalopathy Neuropathologic Changes
- Safety, Tolerability, and Immunogenicity of the ACI-24 Vaccine in Adults With Down Syndrome: A Phase 1b Randomized Clinical Trial
- Beyond the synucleinopathies: alpha synuclein as a driving force in neurodegenerative comorbidities
- Fringe modulates Notch-ligand interactions
- Elevated tauopathy and alpha-synuclein pathology in postmortem Parkinson's disease brains with and without dementia