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 membrane protein TREM2 (Triggering Receptor Expressed on Myeloid cells 2) regulates key microglial functions including phagocytosis and chemotaxis.
Why it matters
In human iPSC-derived microglia, deleting TREM2 caused exaggerated calcium signals in response to purinergic agonists. This is cell-based research, so it is early and does not yet show a treatment for people.
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Neuroinflammation plays a pivotal role in Alzheimer's disease (AD) and Parkinson's disease (PD), the leading causes of dementia.
Why it matters
This perspective describes neuroinflammation as playing a pivotal role in Alzheimer's disease and notes that misfolded proteins activate microglia, leading to synaptic damage and neuronal loss. It states that all proposed drugs so far were based on inhibiting protein aggregation and that targeting the Nrf2 signaling pathway is a potential therapeutic approach.
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Treatment-resistant schizophrenia does not appear to be associated with neuronal, particularly axonal degeneration.
Why it matters
Plasma neurofilament light chain levels did not differ between people with treatment-resistant schizophrenia, their first-degree relatives, people with schizophrenia not on clozapine, and controls. The study found no increase in this marker of neuronal injury in these groups.
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Aging, pathological tau oligomers (TauO), and chronic inflammation in the brain play a central role in tauopathies, including Alzheimer's disease (AD) and frontotemporal dementia (FTD).
Why it matters
This study found that tau oligomers trigger astrocytes to release HMGB1, causing a senescence-like state and inflammation in the brains of people with Alzheimer's disease and frontotemporal dementia, and that blocking HMGB1 release reduced this effect. This is early research and does not yet show whether targeting this process would treat or prevent dementia in patients.
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The histone deacetylase (HDAC) enzymes, a class of epigenetic regulators, are historically well established as attractive therapeutic targets.
Why it matters
This review of HDAC inhibitors found that most clinical trials target hematologic cancers, with an ongoing trend toward other indications including Alzheimer's disease, frontotemporal dementia, and Friedreich's ataxia. It notes that combination regimens can increase treatment-related toxicities and reports no established cure or prevention.
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One hundred forty-six participants were examined (age 72 ± 6 years).
Why it matters
Among 146 older adults, higher aortic stiffness interacted with age on several cerebrospinal fluid markers including p-tau, t-tau, neurogranin and sTREM2. This is an observational association study and does not report a treatment, cure or prevention of Alzheimer's disease.
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Cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP43; also known as TARDBP or TDP-43) is a key pathological feature of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
Why it matters
This review describes how TDP43 is normally controlled through autoregulation, localization and aggregation, and how mislocalization and nuclear loss are linked to ALS and FTD. It is a summary of biology, not a treatment or cure.
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49/100
Obesity-induced white adipose tissue (WAT) hypertrophy is associated with elevated adipose tissue macrophage (ATM) content.
Why it matters
In mice, TREM2 deficiency aggravated diet-induced insulin resistance and hepatic steatosis independently of fat and cholesterol levels. This is an obesity study in animals, so it does not provide evidence about treating, curing or preventing Alzheimer's disease.
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Frontotemporal lobar degeneration proteinopathies with tau inclusions (FTLD-Tau) or TDP-43 inclusions (FTLD-TDP) are associated with clinically similar phenotypes.
Why it matters
In an autopsy cohort, frontotemporal lobar degeneration with tau inclusions and with TDP-43 inclusions showed different patterns of white and grey matter pathology despite similar clinical symptoms. This is a neuropathological study and reports no treatment or prevention.
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Parkinson's disease (PD) is a common neurodegenerative disease associated with accumulation of misfolding proteins and increased neuroinflammation, which may further impair the glymphatic system.
Why it matters
This study used imaging and neuropsychological tests in people with Parkinson's disease to examine glymphatic system activity and its relationship with oxidative stress. It concerns Parkinson's disease, not Alzheimer's disease, and reports no treatment, cure or prevention.
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49/100
Adult-onset neurodegenerative diseases affect millions and negatively impact health care systems worldwide.
Why it matters
This study found a positive link between long-term fine particulate air pollution and first hospitalization for Parkinson's disease, but not for Alzheimer's disease or ALS. It is about pollution exposure and disease aggravation, not treatment or prevention.
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The distinct prion-like domains (PrLDs) of FUS and TDP-43, modulate phase transitions that result in condensates with a range of material states.
Why it matters
This review discusses how the prion-like domains of FUS and TDP-43 control phase transitions and condensates, and how that understanding might be used to design new therapies for ALS, FTD and LATE. It proposes ideas for future treatment but tests none.
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49/100
Alzheimer's Disease (AD), one of the main causes of death in elderly people, is characterized by Mild Cognitive Impairment (MCI) at prodromal stage.
Why it matters
This paper designed a deep network using 18F-FDG PET imaging to identify which people with mild cognitive impairment will develop Alzheimer's disease dementia. It is a prediction method study, so it does not treat, cure, or prevent Alzheimer's disease.
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Human genetic data indicate that microglial dysfunction contributes to the pathology of Alzheimer's disease (AD), exemplified by the identification of coding variants in triggering receptor expressed on myeloid cells 2 (TREM2) and, more recently, in PLCG2, a phospholipase-encoding gene expressed in microglia.
Why it matters
Both TREM2 and PLCG2 carry gene variants linked to Alzheimer's disease, and both are active in microglia, the brain's immune cells. Working with lab-grown human microglia-like cells, this study found that TREM2 signals through PLCγ2 to support cell survival, clearing and processing of neuronal debris, and lipid metabolism, and that PLCγ2 separately drives inflammatory responses through Toll-like receptors. This is lab work on cells, not people. It points to PLCγ2 as a shared control point but does not show a treatment for Alzheimer's disease.
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We screened 3,809 articles and identified 31 eligible studies.
Why it matters
Reviewing 31 studies of gene activity in people with Lewy body dementia, the authors conclude that α-synuclein clumping, mitochondrial dysfunction, faulty clearance of misfolded proteins and RNA-mediated gene silencing contribute to nerve cell damage. They call for larger long-term studies of body fluids to subtype and stage the disease, and say the genes identified need further research as possible diagnostic markers and treatment targets. The work concerns Lewy body dementia rather than Alzheimer's disease.
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BIN1, a member of the BAR adaptor protein family, is a significant late-onset Alzheimer disease risk factor.
Why it matters
In mice, loss of neuronal BIN1 caused impairment in spatial learning and memory and changes in presynaptic neurotransmitter release. This is an animal study and does not show any treatment, cure, or prevention for Alzheimer's disease in humans.
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Loss-of-function genetic variants of triggering receptor expressed on myeloid cells 2 (TREM2) are linked with an enhanced risk of developing dementias.
Why it matters
Using human iPSC-derived microglia, this study found that loss-of-function TREM2 variants lock a metabolic switch, which may impair microglial responses relevant to dementia. It is cell-based laboratory work and does not demonstrate a treatment.
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Microglia mediate multiple facets of neuroinflammation, which plays a double-edged role in various brain diseases via distinct microglial phenotypes (deleterious M1 and neuroprotective M2).
Why it matters
In BV2 microglial cells in vitro, curcumin reduced LPS-induced neuroinflammation and promoted an M2-like microglial state via TREM2/TLR4/NF-κB pathways. This is cell-culture work and does not show that curcumin treats Alzheimer's disease in people.
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Recent interest in enlarged perivascular spaces (ePVS) in the brain, which can be visualized on MRI and appear isointense to cerebrospinal fluid on all sequence weightings, has resulted in the necessity of reliable algorithms for automated segmentation to allow for whole brain assessment of ePVS burden.
Why it matters
This prospective study presents a method to automatically identify enlarged perivascular spaces in white matter using standard 3T T1 and FLAIR MRI, tested in a small dementia-free group and another dataset. It is a technical imaging method and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Mutations in RNA-binding proteins (RBPs) localized in ribonucleoprotein (RNP) granules, such as hnRNP A1 and TDP-43, promote aberrant protein aggregation, which is a pathological hallmark of various neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
Why it matters
This laboratory study investigated how PARylation regulates the assembly and disassembly of RNP granules containing disease-related RNA-binding proteins such as hnRNP A1 and TDP-43. It is mechanistic cell work related to ALS and frontotemporal dementia and does not test a treatment in patients.
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It has been well documented that neurotrophins, including brain-derived neurotrophic factor (BDNF), are severely affected in Alzheimer's disease (AD), but their administration faces a myriad of technical challenges.
Why it matters
In a mouse model of Alzheimer's disease, delivering BDNF from astrocytes improved memory tasks and restored spine density and synaptic properties. This is animal research and does not yet show a treatment, cure, or prevention for people.
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This review recounts the definitions and research evidence supporting the multifaceted roles of neuroinflammation in the injured brain following trauma.
Why it matters
This review of traumatic brain injury describes conflicting protective and detrimental roles of cytokines, leukocytes, and glial cells that might be harnessed therapeutically. It reports no treatment, cure, or prevention for Alzheimer's disease.
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Dysfunction of microglia, the brain's immune cells, is linked to neurodegeneration.
Why it matters
Researchers grew microglia-like immune cells from stem cells of patients with Nasu-Hakola disease, a rare early-onset dementia caused by inheriting two copies of the T66M or W50C TREM2 mutation. Compared with control cells, the mutant cells made and released less TREM2, survived markedly less well, and showed specific deficits in phagocytosis (clearing material), yet their inflammatory cytokine response to LPS was comparable. This is lab cell research on a rare disease, not on Alzheimer's patients, and it does not establish a treatment, cure or prevention for Alzheimer's disease.
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In the initial kindred of ten affected Italian individuals (mean age of disease onset 59·8 years [SD 8·7]), we detected significant linkage of Parkinson's disease to chromosome 14 and nominated LRP10 as the disease-causing gene.
Why it matters
In one Italian family, a region of chromosome 14 was linked to Parkinson's disease and LRP10 was named as a possible disease-causing gene. The findings implicate LRP10 in inherited forms of alpha-synucleinopathies, which are not Alzheimer disease, and do not show a treatment.
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49/100
GWAS found the associations of two single nucleotide polymorphisms (rs7943454 and rs640476) with plasma NFL at suggestive levels.
Why it matters
This genome-wide association study found two loci with suggestive associations with plasma neurofilament light levels in the ADNI-1 cohort. It is about the genetics of a biomarker, not a treatment or cure for Alzheimer's disease.
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.
- Crucial role of calbindin-D28k in the pathogenesis of Alzheimer's disease mouse model
- High capacity and low cost detection of prion protein gene variant alleles by denaturing HPLC
- Cerebrospinal fluid biomarker panel for synaptic dysfunction in a broad spectrum of neurodegenerative diseases
- Severity of dilated Virchow-Robin spaces is associated with age, blood pressure, and MRI markers of small vessel disease: a population-based study
- Segmentation of the mouse hippocampal formation in magnetic resonance images
- The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women
- RNA Binding Antagonizes Neurotoxic Phase Transitions of TDP-43
- Disease-linked TDP-43 hyperphosphorylation suppresses TDP-43 condensation and aggregation
- Increases of SET level and translocation are correlated with tau hyperphosphorylation at ser202/thr205 in CA1 of Ts65Dn mice
- Homozygosity for the C9orf72 GGGGCC repeat expansion in frontotemporal dementia