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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61/100
Why it matters
Reports that long pre-mRNA depletion and RNA missplicing contribute to nerve cell vulnerability from loss of TDP-43.
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Using exome sequencing, we identified a p.R191Q amino acid change in the valosin-containing protein (VCP) gene in an Italian family with autosomal dominantly inherited amyotrophic lateral sclerosis (ALS).
Why it matters
Exome sequencing of one Italian family with inherited ALS found a change in the VCP gene, a gene already known to cause a syndrome combining muscle disease, Paget disease of bone and frontotemporal dementia (IBMPFD). Screening 210 familial and 78 autopsy-confirmed ALS cases found four more VCP mutations, and the authors estimate VCP may account for about 1–2% of familial ALS. The study links ALS to defects in the cell's ubiquitin/protein-disposal pathway; it is about ALS, not Alzheimer's disease, and reports no treatment.
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Imaging patterns of atrophy in CBS vary according to pathologic diagnosis.
Why it matters
In this case-control study of 24 patients with corticobasal syndrome who came to autopsy, different underlying pathologies showed somewhat different patterns of brain atrophy on MRI. It is about predicting pathology in a related syndrome, not about treating, curing, or preventing Alzheimer's disease.
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A slower rate of hippocampal atrophy in normal APOE2 carriers is consistent with the lower risk of Alzheimer disease in these individuals.
Why it matters
In cognitively normal older adults, APOE2 carriers had slower rates of hippocampal atrophy and higher CSF amyloid and lower p-tau than APOE3/3 carriers, but no differences in memory or overall cognitive change were detected. This suggests APOE2 may be protective against some Alzheimer-related brain changes, but it does not show that any treatment can mimic this effect.
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Short-term administration of latrepirdine is well tolerated in patients with HD and may have a beneficial effect on cognition.
Why it matters
In this 90-day trial in people with Huntington disease, latrepirdine was well tolerated and improved mean MMSE scores compared with placebo, but no significant treatment effects were seen on the other measures. It did not test whether the drug treats, cures, or prevents Alzheimer's disease.
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Amyotrophic lateral sclerosis (ALS) is a fatal degenerative motor neuron disorder.
Why it matters
Reports 13 mutations in the FUS/TLS gene on chromosome 16 found in familial amyotrophic lateral sclerosis (ALS), a fatal motor neuron disorder. Mutant FUS/TLS protein built up in the cytoplasm of nerve cells, similar to TDP43, which the authors suggest may be a shared mechanism in ALS and possibly other neurodegenerative disorders.
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61/100
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that is familial in 10% of cases.
Why it matters
Identified mutations in the FUS gene in families with inherited amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease. The authors suggest a mechanism shared with another ALS gene, TARDBP, may underlie motor neuron degeneration. The study is about ALS, not Alzheimer's.
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We identified two variants in TARDBP, which would encode Gly290Ala and Gly298Ser forms of TDP-43, in two kindreds with familial ALS.
Why it matters
Researchers sequenced the TARDBP gene in 259 people with ALS, frontotemporal lobar degeneration or both, and found two variants (Gly290Ala and Gly298Ser) in two families with inherited ALS. The authors judged the variants likely disease-causing because they tracked with illness in both families, were absent in matched controls, and came with TDP-43 brain pathology in the one family with tissue available. They suggest this makes TDP-43 an active driver of nerve-cell damage, not just a by-product. This is a study of ALS, not Alzheimer's disease, and it tests no treatment.
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One of the most challenging problems in modern neuroimaging is detailed characterization of neurodegeneration.
Why it matters
This paper develops and evaluates a brain image registration method for measuring atrophy in elderly and neurodegenerative brains, including in frontotemporal dementia and Alzheimer's disease. It is a technical imaging methods study and does not test any treatment, cure or prevention.
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Reduction of verbal repetition was set as a treatment goal in 44% (n = 57) of randomized patients.
Why it matters
In this secondary analysis of a 4-month trial, more galantamine-treated patients had a reduction in verbal repetition than placebo-treated patients. This concerns a specific symptom goal in mild to moderate Alzheimer's disease and does not show that galantamine cures or prevents it.
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61/100
The recycling of the amyloid precursor protein (APP) from the cell surface via the endocytic pathways plays a key role in the generation of amyloid beta peptide (Abeta) in Alzheimer disease.
Why it matters
This 2007 study reported that inherited variants in the SORL1 gene, found in non-coding (intronic) parts of the gene, are associated with late-onset Alzheimer's disease, and that they "may regulate" how much SORL1 is made. It also showed that SORL1 steers the amyloid precursor protein into recycling pathways, and that when SORL1 is low the protein is sorted into compartments that produce amyloid-beta. The authors say this "suggest[s]" that changes in SORL1 are involved in causing Alzheimer's; our record gives no sample size or effect size, and the study offers no test or treatment.
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Frontotemporal dementia (FTD) is the second most common cause of dementia in people under the age of 65 years.
Why it matters
Some families with frontotemporal dementia (FTD) are linked to the same part of chromosome 17 as the tau gene, yet have no tau-gene mutation and no tau deposits in the brain; this study reports that in these families FTD is caused by mutations in progranulin, a nearby gene for a secreted growth factor, mutations "likely to create null alleles". The authors conclude that this identifies progranulin mutations "as a cause of neurodegenerative disease" and points to the protein's importance for nerve-cell survival. It explains a genetic cause of one form of FTD; its only Alzheimer's link is that progranulin levels rise in activated immune cells in the brain in Alzheimer's and other diseases, and it is not a treatment, cure or prevention.
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In this study, researchers assessed the validity and reliability of an automated labeling system developed to subdivide the human cerebral cortex on magnetic resonance images into gyral based regions of interest.
Why it matters
An automated system for dividing the human cerebral cortex on MRI scans into labelled, gyrus-based regions. It is a measurement tool for brain imaging research and does not treat or prevent Alzheimer's disease.
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61/100
Memory declined in APOE e4 carriers before the symptomatic presentation of MCI in a cohort whose mean age was 60 years over a median period of 33 months.
Why it matters
In 180 cognitively normal volunteers aged 50+ who were followed for about 33 months, people carrying the APOE e4 gene variant showed more decline on verbal memory tests than non-carriers. The study reports this decline "began prior to age 60" and found no differences in language, spatial skills or executive function. These are group averages from newspaper-recruited volunteers: the study cannot predict who will develop Alzheimer's, and it did not test any treatment.
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61/100
In this longitudinal study of 77 patients with mild cognitive impairment (MCI), the authors analyzed whether levels of tau protein phosphorylated at threonine 231 (p-tau(231)) in CSF correlate with progression of cognitive decline.
Why it matters
In this longitudinal study of 77 patients with mild cognitive impairment, high levels of CSF p-tau(231) at baseline correlated with cognitive decline and conversion to Alzheimer's disease, while total tau protein levels did not. The authors conclude that an increased p-tau(231) level is a potential risk factor for cognitive decline in patients with mild cognitive impairment.
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Silent brain infarcts and white matter lesions are frequently seen on magnetic resonance imaging in healthy elderly people and both are associated with an increased risk of stroke and dementia.
Why it matters
In this cross-sectional population study of 1,077 people aged 60 to 90, higher blood levels of homocysteine were associated with silent brain infarcts and more severe white matter lesions, both of which are linked to increased risk of stroke and dementia. Because the study was cross-sectional, it cannot show that lowering homocysteine would prevent these brain changes or dementia.
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The entorhinal cortex (EC) plays a crucial role as a gateway connecting the neocortex and the hippocampal formation.
Why it matters
In this study of 20 brains examined after death, people with the very mildest clinically detectable dementia (CDR 0.5) had 60% fewer layer II neurons in the entorhinal cortex — a gateway to the brain's memory hub — than cognitively normal people, whose counts stayed constant from age 60 to 90; in severe dementia the loss was about 90%. Neuron loss tracked tangles and neuritic plaques but not diffuse plaques, and the authors say this "distinguishes even very mild AD from nondemented aging." All the very mild cases already had enough tangles and plaques for an AD diagnosis, so the study shows how early the damage is found, not what causes it — and it tests no treatment.
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60/100
We found that ApoE4 did not facilitate amyloid-PET-associated ptau increases, suggesting that amyloid-related ptau secretion is not altered by ApoE4 carriage.
Why it matters
This study found that plasma ptau217 elevations were linked to faster tau-PET spread in an ApoE4 allele dose-dependent manner, and that a higher ApoE4 allele count was linked to lower ptau217 thresholds marking transition to tauopathy. It clarifies how the key genetic risk factor for sporadic Alzheimer's disease relates to tau aggregation and spread, but offers no treatment, cure or prevention.
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It was not possible to demonstrate significant differences on the co-primary clinical endpoints (ADAS-cog 11 and ADCS-ADL 23 ) at 52 weeks due to symptomatic activity in the control arm.
Why it matters
This Phase 3 trial could not show significant differences on its main clinical endpoints at 52 weeks because the control arm also showed symptomatic activity. In participants with mild cognitive impairment, some cognitive differences emerged at 78 and 104 weeks, and there were reductions in markers of neurodegeneration and tau pathology.
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Among adults with Down syndrome, the striatum consistently accumulates amyloid earlier than the cortex when measured with PiB.
Why it matters
This longitudinal imaging study found that in adults with Down syndrome, the striatum accumulates amyloid about 3.4 years earlier than the cortex when measured with PiB PET, but florbetapir PET did not detect this early striatal accumulation. It improves understanding of how to detect amyloid onset but does not test any treatment or cure.
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Among 1136 patients in the intention-to-treat population, 526 (46.3%) were female and 610 (53.7%) male; they had a mean (SD) age of 70 (11) years, body mass index of 28 (5), and age-adjusted Charlson Comorbidity Index of 5 (3).
Why it matters
This trial found that indocyanine green fluorescence imaging did not significantly reduce the overall anastomotic leak rate in laparoscopic colorectal surgery. It contains no information on Alzheimer's disease.
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As the brain transitions from wakefulness to sleep, processing of external information diminishes while restorative processes, such as glymphatic removal of waste products, are activated.
Why it matters
This study identified tightly synchronized oscillations in norepinephrine, cerebral blood volume and cerebrospinal fluid as the strongest predictors of glymphatic clearance during NREM sleep, and found that the sleep aid zolpidem suppressed norepinephrine oscillations and glymphatic flow. It describes how sleep architecture drives brain waste clearance, which is relevant to understanding clearance mechanisms but does not test an Alzheimer's treatment, cure or prevention.
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Autophagy is a lysosome-based degradative process used to recycle obsolete cellular constituents and eliminate damaged organelles and aggregate-prone proteins.
Why it matters
This review discusses how problems with autophagy and lysosome function contribute to neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and frontotemporal dementia. It is a review of mechanisms and does not report any treatment, cure, or prevention for Alzheimer's disease.
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We investigated the effects of matrix type and reagent batch changes on diagnostic performances and longitudinal trajectories of brain-derived tau (BD-tau).
Why it matters
This laboratory study found that brain-derived tau measured in plasma and serum gives similar diagnostic accuracy but the absolute values are not interchangeable. It is a technical finding about how to handle blood samples for testing, with no direct implications for treating or preventing Alzheimer's.
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60/100
Loss of nuclear TDP-43 is a hallmark of neurodegeneration in TDP-43 proteinopathies, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
Why it matters
In this laboratory work, blocking a specific splicing event with antisense oligonucleotides restored axonal regeneration and stathmin-2-dependent lysosome trafficking in cells with TDP-43 loss, a mechanism relevant to ALS and frontotemporal dementia. It is early laboratory research and does not test a treatment, cure or prevention 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.
- TDP-43 Mutations in Familial and Sporadic Amyotrophic Lateral Sclerosis
- Metabolic signals and innate immune activation in obesity and exercise
- Overexpression of ABCA1 reduces amyloid deposition in the PDAPP mouse model of Alzheimer disease
- The link between childhood trauma and depression: insights from HPA axis studies in humans
- Population-Scale Integration of Spatial Omics Networks for Clinical Prediction and Biological Discovery by SPIN
- Hippocampal and amygdala volumes according to psychosis stage and diagnosis: a magnetic resonance imaging study of chronic schizophrenia, first-episode psychosis, and ultra-high-risk individuals
- The TREM2-APOE Pathway Drives the Transcriptional Phenotype of Dysfunctional Microglia in Neurodegenerative Diseases
- Suppressive effects of flavonoid fisetin on lipopolysaccharide-induced microglial activation and neurotoxicity
- Effects of Computerized Cognitive Training on Vesicular Acetylcholine Transporter Levels using [18F]Fluoroethoxybenzovesamicol Positron Emission Tomography in Healthy Older Adults: Results from the Improving Neurological Health in Aging via Neuroplasticity-based Computerized Exercise (INHANCE) Randomized Clinical Trial
- CSF lactate levels, τ proteins, cognitive decline: a dynamic relationship in Alzheimer's disease