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.
-
Inclusions of pathogenic deposits containing TAR DNA-binding protein 43 (TDP-43) are evident in the brain and spinal cord of patients that present across a spectrum of neurodegenerative diseases.
Why it matters
This review describes the role of TDP-43 in ALS and frontotemporal lobar degeneration and notes that understanding its disease mechanisms is critical for developing effective therapies. It does not test any treatment or prevention for Alzheimer's disease, so it has no direct implications for treating, curing, or preventing the disease.
-
Pathological hallmarks of Alzheimer's disease (AD) are deposits of amyloid beta (Aβ) and hyper-phosphorylated tau aggregates in brain plaques.
Why it matters
In this small pilot study of cerebrospinal fluid from 13 Alzheimer's, 10 mild cognitive impairment and 10 control samples, three proteins were identified that may help monitor progression from mild cognitive impairment to Alzheimer's. It is early biomarker work and does not show any treatment, cure or prevention.
-
The current review summarizes the current knowledge on longitudinal cortical and subcortical grey and white matter MRI findings assessed using T1-weighted and one-tensor diffusion-weighted MRI in Parkinson's disease (PD) patients.
Why it matters
This review of MRI studies in Parkinson's disease describes progressive brain atrophy and notes that only a few studies used MRI to predict cognitive impairment or dementia conversion. It concerns Parkinson's disease and reports no treatment or prevention results.
-
54/100
Triggering receptor expressed on myeloid cells 2 (TREM2) is essential for the transition of homeostatic microglia to a disease-associated microglial state.
Why it matters
Researchers screened antibodies against TREM2, a receptor on the brain's immune cells, looking for one that stops enzymes from cutting it off the cell surface. One antibody, 4D9, both kept TREM2 on the cell surface and "concomitantly" switched on its internal signalling, helped macrophages survive, and in a living-animal test bound "nearly all soluble TREM2" in cerebrospinal fluid. This shows the antibody reaches its target in the lab and in vivo. It does not show any effect on Alzheimer's pathology or symptoms.
-
Perivascular spaces include a variety of passageways around arterioles, capillaries and venules in the brain, along which a range of substances can move.
Why it matters
This review describes perivascular spaces and their role in clearing fluid and waste from the brain, and notes their involvement in small vessel disease and Alzheimer's disease. It is a review of anatomy, physiology and pathology and reports no treatment that cures or prevents Alzheimer's disease.
-
Dementia is common in Parkinson's disease (PD) but measures that track cognitive change in PD are lacking.
Why it matters
This study used quantitative susceptibility mapping to detect brain iron changes related to cognitive change in Parkinson's disease. It concerns an imaging marker in Parkinson's disease and does not test treating, curing or preventing Alzheimer's disease.
-
The choroid plexus (ChP) is a major source of cerebrospinal fluid (CSF) production, with a direct and indirect role in protein clearance, and pathogenesis of Alzheimer's disease (AD).
Why it matters
In two large datasets, larger choroid plexus volume was associated with lower cerebrospinal fluid protein levels, and this association was weaker in late mild cognitive impairment and Alzheimer's disease patients and in amyloid-positive people. This supports a possible role for the choroid plexus in protein clearance but does not show that any treatment, cure, or prevention works.
-
Dietary habits and vascular risk factors promote both Alzheimer's disease and cognitive impairment caused by vascular factors 1-3 .
Why it matters
In mice, a salt-rich diet induced tau phosphorylation and cognitive dysfunction, and these effects were prevented by restoring endothelial nitric oxide production or by using anti-tau antibodies. This is animal research and does not yet show that reducing salt intake prevents dementia in humans.
-
Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) in cerebrospinal fluid (CSF) has been associated with Alzheimer's disease (AD).
Why it matters
In a genome-wide study of spinal-fluid samples from the Alzheimer's Disease Neuroimaging Initiative, common variants in the MS4A gene region were strongly linked to levels of soluble TREM2, a protein tied to the brain's immune cells (P = 1.15 × 10⁻¹⁵), and this was replicated in independent datasets. The variants that raised soluble TREM2 were associated with lower Alzheimer's risk and later onset, but the record gives no size for either effect. In human macrophages, used as a stand-in for brain immune cells, turning MS4A4A up raised soluble TREM2 and silencing it lowered it, which the authors say "suggest[s] that MS4A4A modulates sTREM2". No treatment was tested.
-
Alzheimer's disease is the most prevalent type of dementia and is caused by the deposition of extracellular amyloid-beta and abnormal tau phosphorylation.
Why it matters
This study reports that systemic inflammation is known to increase the risk for cognitive decline in human neurodegenerative diseases including Alzheimer's, and that microglia change shape once activated. It describes a mechanism involving the NLRP3 inflammasome but reports no treatment, cure or prevention result.
-
Age-related hearing loss (ARHL) has been considered as a promising modifiable risk factor for cognitive impairment and dementia.
Why it matters
This study found that age-related hearing loss was associated with higher cerebrospinal fluid tau levels and brain atrophy over time. It does not show that treating hearing loss prevents dementia, and the findings are from an observational study of biomarkers.
-
Neurodegenerative diseases of the central nervous system progressively rob patients of their memory, motor function, and ability to perform daily tasks.
Why it matters
This is a review of immune signaling pathways, including TREM2, in neurodegeneration. It reports no new treatment, cure, or prevention for Alzheimer's disease.
-
Activation of microglia, the resident immune cells of the central nervous system, is a prominent pathological hallmark of Alzheimer's disease (AD).
Why it matters
This study profiled gene expression in microglia isolated from tau transgenic mice across four age groups to see what changes accompany microglial activation in response to tau pathology. It is animal research only and reports no treatment, cure or prevention for people.
-
Alzheimer disease (AD) is a debilitating dementia believed to result from the deposition of extracellular amyloid-β (Aβ)-containing plaques followed by the formation of neurofibrillary tangles.
Why it matters
Variations in the TREM2 gene, which is expressed in microglia in the brain, have been shown to increase the risk of developing late-onset Alzheimer's disease. This identifies a genetic risk factor and a role for microglia, but it does not yet provide a treatment or cure.
-
As serum NfL correlates with functional impairment and brain atrophy in bvFTD at different disease stages, we propose it as marker of disease severity, paving the way for its future use as outcome measure for clinical trials.
Why it matters
In this study, serum neurofilament light chain was higher in people with behavioral variant frontotemporal dementia than in Alzheimer disease, mild cognitive impairment, or healthy controls, and it rose over time in bvFTD and AD. It correlated with functional decline and brain atrophy in bvFTD, but the study does not test any treatment, cure, or prevention.
-
Alzheimer's disease is characterized by the histopathological presence of amyloid-β plaques and tau-containing neurofibrillary tangles.
Why it matters
In people with mild cognitive impairment and Alzheimer's disease, brain imaging showed that microglial activation was correlated with both tau and amyloid accumulation. This suggests all three processes increase together, but the study does not show that targeting them prevents or treats the disease.
-
Aging is a major risk factor for both genetic and sporadic neurodegenerative disorders.
Why it matters
This mouse and human brain study found that aging reduces TAK1 expression, which cooperates with genetic risk factors to promote the onset of ALS/FTD, and that these features were blocked upon inhibition of RIPK1 in mice. These are early animal and tissue findings about ALS and frontotemporal dementia, not a treatment, cure or prevention for Alzheimer's disease.
-
Neurodegenerative disorders of ageing (NDAs) such as Alzheimer disease, Parkinson disease, frontotemporal dementia, Huntington disease and amyotrophic lateral sclerosis represent a major socio-economic challenge in view of their high prevalence yet poor treatment.
Why it matters
This article discusses emerging mechanisms for promoting the clearance of toxic proteins as a possible way to delay the onset or slow the progression of neurodegenerative disorders including Alzheimer's disease. It is a discussion of strategy, not a tested treatment, cure or prevention.
-
To what extent does the subarachnoid cerebrospinal fluid (CSF) compartment communicate directly with the extravascular compartment of human brain tissue?
Why it matters
Using an injected tracer and MRI, this study showed that a substance given into the spinal fluid reached all regions of the human brain, and that its clearance was delayed in a group of patients with dementia. It is an early look at how fluid moves through the brain and does not test any treatment, cure or prevention.
-
We observed three stages of activity during both visual picture naming and auditory naming to definition that were serially organized: sensory processing, lexical semantic processing, and articulation.
Why it matters
This study mapped three stages of brain activity during naming tasks and identified brain regions involved in processing word meaning. It describes how the healthy brain handles language and does not test any treatment, cure, or prevention for Alzheimer's disease.
-
54/100
Cytoplasmic FUS aggregates are a pathological hallmark in a subset of patients with frontotemporal dementia (FTD) or amyotrophic lateral sclerosis (ALS).
Why it matters
This laboratory work identifies two mechanisms—Transportin binding and arginine methylation—that normally keep the FUS protein from clumping, and shows these are weakened in FUS-related FTD and ALS. It is early, cell-based research and does not test any treatment in patients.
-
Description The American College of Physicians developed this guidance statement to guide clinicians in selecting targets for pharmacologic treatment of type 2 diabetes.
Why it matters
This guidance statement concerns blood sugar targets for treating type 2 diabetes in adults, not Alzheimer's disease. It recommends personalising glycemic goals and aiming for an HbA1c level between 7% and 8% in most patients.
-
Hypertension is a major risk factor for many common chronic diseases, such as heart failure, myocardial infarction, stroke, vascular dementia, and chronic kidney disease.
Why it matters
This review describes mechanisms of vascular smooth muscle contraction in hypertension, a condition listed as a risk factor for vascular dementia. It does not test or report any treatment, cure, or prevention for Alzheimer's disease.
-
The diagnosis and treatment of synucleinopathies such as Parkinson disease and dementia with Lewy bodies would be aided by the availability of assays for the pathogenic disease-associated forms of α-synuclein (αSyn D ) that are sufficiently sensitive, specific, and practical for analysis of accessible diagnostic specimens.
Why it matters
This study describes an improved laboratory test that detects disease-associated alpha-synuclein seeds in cerebrospinal fluid in 1-2 days, with 93% sensitivity and 100% specificity in the samples tested so far. It is a diagnostic test for synucleinopathies such as Parkinson's disease and dementia with Lewy bodies, not a treatment or cure.
-
In a cross-sectional design, pathology was confirmed by autopsy or a pathologically validated CSF total tau-to-β-amyloid ratio (T-tau/Aβ).
Why it matters
This study used brain imaging to look at how the source of nerve cell damage affects brain network efficiency in people with corticobasal syndrome, distinguishing Alzheimer's from non-Alzheimer's degeneration. It is a cross-sectional study and does not test any treatment or cure.
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 single dose of a vectorized mAb targeting TDP-43 potently inhibits the neuropathology in a model of ALS/FTD
- Diffusion tensor imaging of cingulum fibers in mild cognitive impairment and Alzheimer disease
- Correlation of cerebrospinal fluid levels of tau protein phosphorylated at threonine 231 with rates of hippocampal atrophy in Alzheimer disease
- Transient cerebral ischemia induces aberrant neuronal cell cycle re-entry and Alzheimer's disease-like tauopathy in female rats
- Diagnostic performance of cerebrospinal fluid total tau and phosphorylated tau in Creutzfeldt-Jakob disease: results from the Swedish Mortality Registry
- Trem2 promotes anti-inflammatory responses in microglia and is suppressed under pro-inflammatory conditions
- Caspase-1 inhibition alleviates cognitive impairment and neuropathology in an Alzheimer's disease mouse model
- AAVrh.10 delivery of novel APOE2-Christchurch variant suppresses amyloid and Tau pathology in Alzheimer's disease mice
- Age-related shift in LTD is dependent on neuronal adenosine A2A receptors interplay with mGluR5 and NMDA receptors
- Indocyanine Green Fluorescence Imaging in Prevention of Colorectal Anastomotic Leakage