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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Cerebrospinal fluid (CSF) synaptosomal-associated protein 25 (SNAP-25) and neurogranin (Ng) are recently described biomarkers for pre- and postsynaptic integrity known to be elevated in symptomatic Alzheimer disease (AD).
Why it matters
Among 274 cognitively normal people, those carrying the APOE ε4 risk variant had higher levels of the presynaptic marker CSF SNAP-25, but not the postsynaptic marker neurogranin, even after adjusting for amyloid status. This is a biomarker observation and does not show that measuring or changing SNAP-25 affects the development of Alzheimer disease.
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Animal work investigating the consequences of maternal high-fat diet (mHFD) revealed in the offspring a maternal immune activation (MIA) phenotype associated with increased inflammatory signals.
Why it matters
This animal study examined microglial and peripheral immune priming in adolescent mouse offspring exposed to maternal high-fat diet. It is mouse research on developmental immune effects and does not report any treatment, cure, or prevention for Alzheimer's disease.
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NLR may be useful to identify and stratify patients who could benefit from adjunctive anti-inflammatory treatment.
Why it matters
This cross-sectional study compared a marker of systemic inflammation across psychiatric diagnoses, including dementia. It found elevated levels in several diagnoses including dementia, but it does not show that this marker causes or can be treated to affect Alzheimer's disease.
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Pattern expression strengths predicted amyloid status with a sensitivity of 0.94 and a specificity of 0.83.
Why it matters
A single flortaucipir PET scan distinguished amyloid-positive from amyloid-negative neurodegenerative disease with high accuracy, and the authors suggest it may also provide information on amyloid, tau and neurodegeneration status. This concerns diagnosis only and does not treat, cure or prevent Alzheimer's disease.
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Microglia are brain macrophages that mediate neuroinflammation and contribute to and protect against neurodegeneration.
Why it matters
This review describes how sialylation on cells can inhibit microglial phagocytosis and inflammatory activation through receptors such as Siglecs. It is a conceptual overview and does not report a treatment, cure, or prevention for Alzheimer's disease.
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Accumulating evidence from animal and human studies supports the notion that physical exercise can enhance neuroplasticity and thus reduce the risk of several neurodegenerative diseases (e.g., dementia).
Why it matters
This review summarizes evidence that lactate and BDNF may mediate some effects of exercise on neuroplasticity, based on findings such as increased peripheral lactate being associated with increased peripheral BDNF. It does not show that lactate or BDNF can treat, cure or prevent Alzheimer's disease.
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Neurodegenerative diseases, including Alzheimer, Parkinson, Huntington, and amyotrophic lateral sclerosis, are a prominent class of neurological diseases currently without a cure.
Why it matters
This paper reviews shared molecular and cellular pathologies across neurodegenerative diseases and asks whether metabolic deficiency is the root cause. It is a conceptual review and reports no treatment, cure or prevention for Alzheimer's disease.
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46/100
One-hundred nineteen individuals with a family history of AD (Presymptomatic Evaluation of Experimental or Novel Treatments of Alzheimer's Disease [PREVENT-AD] cohort, mean age 67 ± 5 years) underwent tau-PET ([ 18 F]FTP), β-amyloid (Aβ)-PET ([ 18 F]NAV4694 [NAV]), and cognitive assessment.
Why it matters
In 119 asymptomatic adults with a family history of Alzheimer's disease, intermediate flortaucipir uptake was associated with amyloid PET and cerebrospinal fluid tau. This is an observational study and does not show that any intervention changes these markers or prevents dementia.
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Several genetic variants of the Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) have been shown to increase the risk of developing Alzheimer's disease (AD) supporting a role of microglia and immune cells in the pathobiology of AD.
Why it matters
Using an engineered cell model, this study found that shedding of the TREM2 N-terminal domain blocked phagocytosis but did not affect TREM2's inhibition of NFkB activation. This is laboratory cell work on signaling and does not show a treatment, cure, or prevention for Alzheimer's disease.
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Advances in human genetics have implicated a growing number of genes in neurodegenerative diseases, providing insight into pathological processes.
Why it matters
This review summarizes genetic evidence that microglial cells contribute to Alzheimer's disease and other neurodegenerative conditions. It highlights microglia as possible targets for future therapies, but it is a summary of research and not a treatment or cure.
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Metals are involved in different pathophysiological mechanisms associated with neurodegenerative diseases (NDDs), including Alzheimer's disease (AD), Parkinson's disease (PD) and multiple sclerosis (MS).
Why it matters
This review reports that low zinc and high copper, manganese, and iron are involved in inflammatory, oxidative, and nitrosative stress pathways linked to neurodegeneration, and that high copper, manganese, and iron participate in forming alpha-synuclein aggregates in Lewy bodies. In Alzheimer's disease, low zinc suppresses beta-amyloid-induced neurotoxicity while high zinc may enhance fibrillar beta-amyloid aggregation, but the review does not establish a treatment or cure.
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Down syndrome is the most common genetic developmental disorder in humans and is caused by partial or complete triplication of human chromosome 21 (trisomy 21).
Why it matters
This review discusses how brain imaging and Down syndrome mouse models are being used to find possible targets for treatment that could improve the growth of new brain cells and long-term thinking. It suggests that Down syndrome could become one of the first genetic disorders treated before birth to try to normalize brain development, but this is a hope for the future, not a current treatment.
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46/100
Concentrations of phosphorylated tau181, total tau (t-tau), and β-amyloid in the CSF were measured in 3 groups: 22 former professional athletes with multiple concussions (mean ± SD age 55.9 ± 12.2 years), 5 healthy controls (age 57.4 ± 5.2 years), and 12 participants (age 60.0 ± 6.6 years) diagnosed with Alzheimer disease (AD).
Why it matters
Former professional athletes with multiple concussions had elevated cerebrospinal fluid total tau, which the study related to white matter integrity and cognitive performance. It is a biomarker study in a small group, so it does not show how to treat, cure or prevent Alzheimer's disease.
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Tumor-infiltrating myeloid cells are the most abundant leukocyte population within tumors.
Why it matters
This study used single-cell RNA sequencing to examine myeloid cell composition and transcriptional dynamics in tumor and adjacent normal tissue from four early-stage lung cancer patients. It concerns cancer, not Alzheimer's disease, and provides no information about treating, curing or preventing Alzheimer's disease.
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People with Down syndrome (DS) are at high risk of developing Alzheimer disease (AD) with aging.
Why it matters
In 24 adults with Down syndrome and 24 controls, plasma neurofilament light was higher in the Down syndrome group and higher levels were linked to decreased adaptive behavior one year later. This is a small study suggesting a possible prognostic blood marker, not a treatment or prevention.
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ANOVA revealed significant group differences in lateral ventricular SUVR across the Alzheimer, mild cognitive impairment, and healthy control groups ( P = 0.004).
Why it matters
Using dynamic 11C-PiB PET, this study found lower lateral ventricular signal and lower clearance of the tracer out of the lateral ventricles in Alzheimer's patients than in healthy controls, with similar findings in mild cognitive impairment and multiple sclerosis. This suggests a method to observe cerebrospinal fluid flow changes in Alzheimer's, but it does not test treatment, cure or prevention.
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Murine microglia expressing the Alzheimer's disease-linked TREM2 R47H mutation display variable decrease in phagocytosis, while impaired phagocytosis is reported following loss of TREM2.
Why it matters
Human stem cell-derived monocytes and microglia-like cells with loss of TREM2 showed impaired clearance of amyloid plaques. This is a cell-based laboratory study and does not yet show a treatment, cure, or prevention for Alzheimer's disease in people.
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Alzheimer's disease (AD) is a late-onset dementia characterized by the deposition of amyloid plaques and formation of neurofibrillary tangles (NFTs) which lead to neuronal loss and cognitive deficits.
Why it matters
This review discusses how TREM2 affects microglia in Alzheimer's disease and notes that whether the glial response is helpful or harmful is still debated. As a review, it summarizes existing research and does not itself show that any treatment prevents or cures Alzheimer's disease.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is an immune receptor expressed on the surface of microglia, macrophages, dendritic cells, and osteoclasts.
Why it matters
This structural biology study describes how the R47H TREM2 variant changes the shape of the receptor, helping explain its loss of function. It is laboratory-based molecular work and does not test any treatment or prevention in people.
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46/100
Alzheimer's disease (AD) has been genetically and pathologically associated with neuroinflammation.
Why it matters
This study notes that a soluble cleavage product of TREM2 is elevated in Alzheimer's disease and asks whether it relates to markers of inflammation. It is about biomarkers and does not report any treatment, cure, or prevention.
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Eukaryotic cells contain distinct organelles, but not all of these compartments are enclosed by membranes.
Why it matters
This laboratory study describes how liquid-liquid phase separation of TDP-43 is mediated by just a few aromatic residues. It is basic biochemistry and does not show any treatment, cure or prevention for Alzheimer's disease.
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Administration of exosomes derived from mesenchymal stromal cells (MSCs) could improve some neurologic conditions by transferring functional biomolecules to recipient cells.
Why it matters
In transgenic APP/PS1 mice, exosomes from mesenchymal stromal cells, especially hypoxia-preconditioned ones, were reported to improve cognitive decline by rescuing synaptic dysfunction and regulating inflammatory responses. This is animal research only and does not establish a treatment for people with Alzheimer's disease.
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Over the course of most common neurodegenerative diseases the amygdala accumulates pathologically misfolded proteins.
Why it matters
This review suggests the amygdala may be a preferential site where multiple misfolded proteins accumulate and where a transition to more aggressive disease may occur. It is a review of autopsy and other data, not a treatment trial, and the authors describe the amygdala as complex and imperfectly defined.
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative diseases with overlap in clinical presentation, neuropathology, and genetic underpinnings.
Why it matters
This study performed mass spectrometry-based proteomic analysis of frontal cortical tissues from postmortem cases of ALS, FTD, ALS/FTD, and controls, including some with the C9orf72 expansion mutation. It is a postmortem proteomic study of the ALS-FTD spectrum and does not report a treatment or cure.
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Test-retest analyses demonstrated low variability in flortaucipir F 18 SUVR.
Why it matters
This test-retest study found that the tau PET imaging agent flortaucipir F 18 had low variability across brain regions, suggesting it could be used to examine changes in tau burden over time. It is a technical imaging study, not a test of treating, curing, or preventing 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.
- The relationship between neurological disease and bullous pemphigoid: a population-based case-control study
- Atorvastatin therapy lowers circulating cholesterol but not free radical activity in advance of identifiable clinical benefit in the treatment of mild-to-moderate AD
- Lamotrigine and Stevens-Johnson Syndrome Prevention
- Increased localization of APP-C99 in mitochondria-associated ER membranes causes mitochondrial dysfunction in Alzheimer disease
- Basal Forebrain Volume, but Not Hippocampal Volume, Is a Predictor of Global Cognitive Decline in Patients With Alzheimer's Disease Treated With Cholinesterase Inhibitors
- Lewy bodies and parkinsonism in families with parkin mutations
- C9orf72 is required for proper macrophage and microglial function in mice
- Microglial activation in the right amygdala-entorhinal-hippocampal complex is associated with preserved spatial learning in AppNL-G-F mice
- Neurodegenerative changes including altered tau phosphorylation and neurofilament immunoreactivity in mice transgenic for the serine/threonine kinase Mos
- CXCR-4 (Fusin), a co-receptor for the type 1 human immunodeficiency virus (HIV-1), is expressed in the human brain in a variety of cell types, including microglia and neurons