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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We found cortical regions where a reduced glucose metabolism was maximally correlated with distributed patterns of tau, accounting for the effect of Aβ and APOE ε4 genotype.
Why it matters
This imaging study found that reduced glucose metabolism in the brain was more strongly correlated with tau protein patterns than with amyloid-beta, independent of APOE ε4 genotype. The results suggest tau plays a more significant role than amyloid-beta in this metabolic change, but the study is observational and does not test a treatment.
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Tauopathies are a group of neurodegenerative diseases characterized by the alteration/aggregation of TAU protein.
Why it matters
Levels of RIPK1 were elevated in mouse models and human tissue from several tau-related disorders, and a RIPK1 inhibitor reduced reactive astrocytes in a mouse model but did not protect against neurodegeneration. This suggests that blocking RIPK1 may reduce some inflammation but is not sufficient on its own to stop nerve cell loss.
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This study demonstrates that Pdpn exerts a novel player in T2DM-induced neuroinflammation and cognitive decline.
Why it matters
In mice with type 2 diabetes, knocking down the Pdpn gene in astrocytes improved memory impairment and reduced hippocampal inflammatory factors. This is early animal research on diabetes-related vascular dementia, not a treatment for Alzheimer's disease.
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38/100
Alzheimer’s disease (AD), the most prevalent form of dementia in the elderly, involves critical changes such as reduced aerobic glycolysis in astrocytes and increased neuronal apoptosis, both of which are significant in the disease’s pathology.
Why it matters
In astrocytes exposed to amyloid-beta in the laboratory, the SENP1/PUM2/NRF2 pathway reduced glycolysis and increased neuronal apoptosis, and targeting this pathway in transgenic mice increased glycolytic enzymes. These are early cell and animal findings that identify potential targets, not a proven treatment.
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38/100
For over a century after their discovery astrocytes were regarded merely as cells located among other brain cells to hold and give support to neurons.
Why it matters
This review discusses evidence that astrocytes are heterogeneous subpopulations that differ in molecular signature and function, and proposes them as druggable targets in aging and Alzheimer's disease. It is a review of cell biology and does not demonstrate a treatment, cure or prevention.
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Only the real-tACS group improved in the oddball task and exhibited increased event-related EEG amplitude in the theta range.
Why it matters
This study found that only the group receiving real transcranial alternating current stimulation improved on an oddball task and showed increased theta-range EEG activity. It is a small study and does not show whether this stimulation prevents or treats Alzheimer's disease.
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We found ADI*pTau217 interactions on immediate and delayed word recall.
Why it matters
In this small cohort of 136 adults, higher neighborhood disadvantage and several plasma biomarkers were each linked to worse cognition, and neighborhood disadvantage changed the link between pTau217 and memory. It is an early biomarker study and does not test any treatment, cure or prevention.
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Clinical studies have shown that epileptic seizures worsen Alzheimer's disease (AD) pathology and related cognitive deficits; however, the underlying mechanism is unclear.
Why it matters
In 5×FAD mice, induced seizures increased Alzheimer-like brain pathology, and an ERK inhibitor reduced some of these changes. This is an animal study, so it does not establish any treatment or prevention for people with Alzheimer's disease.
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Our results provide further insights into the architecture and underlying mechanisms of complex rearrangements on acrocentric chromosomes.
Why it matters
Using short-read and long-read sequencing, this study resolved three complex chromosome 21 rearrangements and found a region between 21p13 and 21p12 frequently involved, with acrocentric satellite DNA at several breakpoints. It is a genomics study of chromosome structure and reports no treatment, cure or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is a commonly reported neurodegenerative disorder associated with dementia and cognitive impairment.
Why it matters
This paper describes microglial activation and immunological dysfunction as having a profound role in the pathogenesis of Alzheimer's disease, involving signalling pathways such as Nrf2/NLRP3/NF-kB/p38 MAPKs/GSK-3β. It discusses the potential neuroprotective role of plant compounds, but reports no proven treatment.
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Most Alzheimer disease (AD) patients present as sporadic late onset AD, with metabolic factors playing an important role in the occurrence and development of AD.
Why it matters
In mice expressing mutant human tau, a long-term high fat diet produced metabolic disorders and worsened behavioral and cognitive deficits. This is an animal study and does not show that diet changes would treat or prevent Alzheimer disease in people.
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Reducing Alzheimer disparities and generating the evidence needed to promote brain health for everyone requires diverse research representation, including areas near an ADRC.
Why it matters
This study found that people with more neighborhood disadvantage and more Alzheimer's-related brain changes at death were less likely to have lived near a brain donation center. It is about research participation and brain donation, not about treating, curing, or preventing Alzheimer's disease.
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This study provides new insights into the regional binding distribution of a first-generation and a second-generation Tau tracer in limbic and neocortical regions in adults with DS, as well as regional differences in Tau binding in adult with DS vs. those with AD.
Why it matters
In postmortem brain tissue from adults with Down syndrome and Alzheimer's disease, two tau PET tracers bound to tau deposits and correlated with AT8 immunostaining, with some differences between the tracers. This is laboratory work on tracer binding and does not treat, cure or prevent Alzheimer's disease.
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Alzheimer's disease (AD) is a neurodegenerative disorder without a known cure or effective treatment.
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Down syndrome (DS), the most common cause of intellectual disability of genetic origin, is characterized by alterations in central nervous system morphology and function that appear from early prenatal stages.
Why it matters
This review describes how the neuropathological events of Alzheimer's disease appear to be interrelated through feedback mechanisms, in people with and without Down syndrome. It is a summary of proposed signalling pathways rather than a test of any treatment, so it does not show that any therapy works.
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Erythrocytes are deeply sensitive cells and important health indicators.
Why it matters
This review describes how red blood cells are affected by oxidative stress and how their membrane changes and enzyme activity might be measured in conditions including Alzheimer's disease. It proposes these red blood cell measures as possible tools for studying and monitoring oxidative stress related diseases, but reports no treatment or cure.
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Hypertension is a leading cause of stroke and dementia, effects attributed to disrupting delivery of blood flow to the brain.
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38/100
Previous research has demonstrated beneficial impact of spermidine intake on memory functions in both animal models and humans, suggesting that spermidine may be a preventive approach to delay age-related cognitive decline and possibly even Alzheimer's disease (AD).
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Our lab has recently shown that the Sigma-2 Receptor/Transmembrane Protein 97 (TMEM97) and Progesterone Receptor Membrane Component 1 (PGRMC1) form a complex with the Low Density Lipoprotein Receptor (LDLR), and this intact complex is required for efficient uptake of lipoproteins such as LDL and apolipoprotein E (apoE).
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Deposition of hyperphosphorylated and aggregated tau protein in the central nervous system is characteristic of Alzheimer disease and other tauopathies.
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Accumulating evidence suggests that inflammation is a major contributor in the pathogenesis of several highly prevalent, but also rare, neurological diseases.
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The apolipoprotein E ( APOE ) ε4 allele is the strongest genetic risk factor for late-onset Alzheimer's disease mainly by driving amyloid-β pathology.
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38/100
Mutations in the GBA1 gene are the most common genetic risk factor for Parkinson's disease (PD) and dementia with Lewy bodies (DLB).
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FUS is a nuclear RNA-binding protein, and its cytoplasmic aggregation is a pathogenic signature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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Reduced spine densities and age-dependent accumulation of amyloid β and tau pathology are shared features of Down syndrome (DS) and Alzheimer's disease (AD).
Why it matters
This study found reduced levels of two actin regulatory proteins at synapses in people with Down syndrome plus Alzheimer pathology and in people with Alzheimer disease alone. It did not find a correlation between one of these proteins and tau pathology, and it does not test any treatment or cure.
From across this topic
9 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 9. The same 9 appear here every time.
- TOMM40'523 variant and cognitive decline in older persons with APOE ε3/3 genotype
- Key Aging-Associated Alterations in Primary Microglia Response to Beta-Amyloid Stimulation
- Contributions of genetic risk and fetal hypoxia to hippocampal volume in patients with schizophrenia or schizoaffective disorder, their unaffected siblings, and healthy unrelated volunteers
- Progression of grey and white matter brain damage in Parkinson's disease: a critical review of structural MRI literature
- The miR-124 regulates the expression of BACE1/β-secretase correlated with cell death in Alzheimer's disease
- Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria
- Stimulation of TREM2 with agonistic antibodies-an emerging therapeutic option for Alzheimer's disease
- TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer's Disease
- A proteo-transcriptomic map of non-alcoholic fatty liver disease signatures