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 have previously reported a large Danish pedigree with autosomal dominant frontotemporal dementia (FTD) linked to chromosome 3 (FTD3).
Why it matters
This 2005 study looked for the gene behind frontotemporal dementia (FTD) that was passed down through a large Danish family. It found a change in a gene called CHMP2B that disrupted how the gene's message was processed in tissue from affected family members, and a second CHMP2B change in one unrelated person with FTD. The authors propose that faults in the "ESCRTIII complex" "may" cause FTD; it is a finding from one family and one other person, and it is about frontotemporal dementia, not Alzheimer's or Lewy body dementia.
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We have previously linked families with autosomal-dominant, late-onset parkinsonism to chromosome 12p11.2-q13.1 (PARK8).
Why it matters
This genetic study found six disease-segregating mutations in LRRK2 in families with autosomal-dominant, late-onset parkinsonism, with diverse brain pathologies at post mortem. It concerns parkinsonism and related disorders, not the treatment, cure or prevention of Alzheimer's disease.
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The frontal lobes are most severely affected by SIVD.
Why it matters
In 78 subjects, white matter lesions in frontal and parietal regions were associated with reduced frontal glucose metabolism, and lesions in all brain regions were associated with low executive scores in nondemented subjects. Regardless of location, these lesions were associated with frontal hypometabolism and executive dysfunction.
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The APOE-4 allele increases risk and decreases age at onset of PD, an association that may not be dependent upon cognitive impairment.
Why it matters
In this family-based genetic study, the APOE-4 allele was associated with increased risk and earlier age at onset of Parkinson disease, while the APOE-3 allele was associated with decreased risk. This concerns Parkinson disease rather than Alzheimer's disease and does not report a treatment, cure, or prevention for either.
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57/100
These data support distinct processes in the initiation and progression of AD pathology within the temporal cortex: Deposition of Abeta reaches a "ceiling" early in the disease process, whereas NFT formation, synaptic loss, and gliosis continue throughout the course of the illness.
Why it matters
In post-mortem tissue from one temporal-lobe region of 83 Alzheimer's and 26 control brains, amyloid was markedly increased even when dementia had been short, and its level did not vary with how long dementia had lasted. Tangles, synaptic loss (lower synaptophysin) and gliosis (higher GFAP) were all greater the longer the illness. The authors conclude that amyloid "reaches a 'ceiling' early" while the other damage continues. Each brain was measured once after death, so this is an association between people, not a cause-and-effect sequence, and no treatment was tested.
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This study performed an anatomical parcellation of the MNI spatially normalized single-subject high-resolution T1 volume by delineating main sulci as landmarks to define 45 anatomical volumes of interest (AVOI) in each hemisphere.
Why it matters
Describes a method for automatically labeling brain areas in SPM brain imaging analyses, based on an anatomical map of a single MRI brain.
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JNPL3 transgenic mice expressing a mutant tau protein, which develop neurofibrillary tangles and progressive motor disturbance, were crossed with Tg2576 transgenic mice expressing mutant beta-amyloid precursor protein (APP), thus modulating the APP-Abeta (beta-amyloid peptide) environment.
Why it matters
Crossing mice that make a mutant tau protein with mice that make mutant APP produced offspring with substantially more neurofibrillary tangle pathology in the limbic system and olfactory cortex than the tau-only mice. The authors say APP or amyloid-beta influences tangle formation, which supports the hypothesis that a similar interaction occurs in Alzheimer's disease.
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Familial multiple system tauopathy with presenile dementia (MSTD) is a neurodegenerative disease with an abundant filamentous tau protein pathology.
Why it matters
A mutation in the tau gene was found in familial multiple system tauopathy with presenile dementia, along with an abnormal preponderance of four-repeat over three-repeat tau isoforms that formed abnormal tau filaments. This shows that dysregulated tau production can cause neurodegeneration, but it is a genetic finding with no treatment tested.
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To improve the specificity and sensitivity of the clinical diagnosis of progressive supranuclear palsy (PSP, Steele-Richardson-Olszewski syndrome), the National Institute of Neurological Disorders and Stroke (NINDS) and the Society for PSP, Inc. (SPSP) sponsored an international workshop to develop an accurate and universally accepted set of criteria for this disorder.
Why it matters
Sets out the NINDS-SPSP criteria for diagnosing progressive supranuclear palsy (PSP), with three levels of certainty: possible, probable and definite. The probable criteria are highly specific but not very sensitive, while the possible criteria are more sensitive but less specific.
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From clinically based series it has been proposed that, in homozygotes for the apolipoprotein E epsilon 4 (apoE epsilon 4) allele, Alzheimer's disease is almost inevitable by the age of 80.
Why it matters
In a population sample of people aged 70 and over, having an apolipoprotein E epsilon 4 allele was linearly associated with both dementia and cognitive impairment. It reports a genetic association and does not show that any treatment, cure or prevention is available.
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Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited arterial disease of the brain recently mapped to chromosome 19.
Why it matters
This study describes the clinical spectrum of CADASIL, an inherited arterial disease of the brain that can cause dementia. It is about a hereditary cause of stroke and dementia, not about treating, curing or preventing Alzheimer's disease.
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Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) has been recently reported as a cause of stroke.
Why it matters
This genetic linkage study mapped the disease locus for CADASIL, a cause of stroke that can lead to dementia, to chromosome 19q12. It concerns a specific inherited small vessel disease, not Alzheimer's disease treatment, cure or prevention.
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Apolipoprotein E is a plasma protein that serves as a ligand for low density lipoprotein receptors and, through its interaction with these receptors, participates in the transport of cholesterol and other lipids among various cells of the body.
Why it matters
Describes apolipoprotein E, a blood protein that helps carry cholesterol and other fats between cells, and its roles in repair after nerve injury, immune regulation and cell growth. The summary does not discuss Alzheimer's disease.
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56/100
Characterizing the timing and progression of Alzheimer's disease biomarker onset in Down syndrome (DS) and contrasting potential timing differences with neurotypical adults is needed to identify optimal Alzheimer's disease therapeutic treatment windows in DS.
Why it matters
In adults with Down syndrome, beta-amyloid plaques, p-tau217 and tau tangles became positive at earlier ages and with less time between them than in neurotypical adults. The authors state this highlights the need for early therapeutic interventions in this population, though no treatment itself was tested.
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Nuclear depletion and cytoplasmic aggregation of the RNA-binding protein TDP-43 are cellular hallmarks of amyotrophic lateral sclerosis (ALS).
Why it matters
This laboratory study found that loss of TDP-43 in stem cell-derived neurons causes cryptic alternative polyadenylation events, which were also seen in ALS and frontotemporal dementia brain tissue. It identifies a newly described consequence of TDP-43 loss but does not test any treatment, prevention or cure.
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ARIA-positive patients had significantly higher Fazekas scores compared with ARIA-negative patients (1.37 versus 1.0; P = .0262), indicating a greater DWMH burden.
Why it matters
In this cohort, patients who developed amyloid-related imaging abnormalities had higher deep white matter hyperintensity burden as measured by the Fazekas score, which was a significant predictor of ARIA. The authors say larger studies with more vascular biomarkers are needed before this can be used to stratify risk.
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Extracellular vesicles (EVs) in plasma are composed of exosomes, microvesicles, and apoptotic bodies.
Why it matters
A magnetic bead method called Mag-Net enriched extracellular vesicles from plasma and found 204 proteins that differed between people with Alzheimer's disease dementia and those without, distinguishing the groups with an area under the curve of 0.98 in a pilot cohort. This is an early, small study of a detection method and does not treat, cure or prevent Alzheimer's disease.
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Sensitivity analyses were performed to validate the robustness of the linear regression results.
Why it matters
Greater handgrip strength was linked to less white matter hyperintensity volume and less white matter injury, with testosterone partly mediating this relationship. This is an observational finding and does not show that increasing handgrip strength or testosterone prevents dementia.
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The aetiology of HS-A is heterogeneous, but HS-A is strongly associated with limbic-predominant age-related TDP-43 encephalopathy NC (LATE-NC).
Why it matters
In this neuropathology study, limbic-predominant age-related TDP-43 encephalopathy was strongly associated with hippocampal sclerosis of ageing, and cerebrovascular changes were also associated with it independently of LATE-NC. These are associations found in brain tissue and do not establish any treatment or prevention.
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Plasma p-tau212 might have utility for theragnostics, monitoring therapy efficacy, and as a target engagement biomarker in clinical trials both in sporadic and DSAD.
Why it matters
Plasma p-tau212 was increased in people with Down syndrome and in sporadic Alzheimer's disease, including prodromal and mild cognitive impairment states, and began rising around when amyloid PET became positive. The authors suggest it might be useful for monitoring therapy efficacy and as a target engagement biomarker in trials, but no treatment was tested here.
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Cerebral small vessel disease (SVD) is recognized as a major vascular contributor to cognitive decline, ultimately leading to dementia and stroke.
Why it matters
This review discusses how dysfunction of waste clearance involving perivascular spaces may contribute to cerebral small vessel disease, and notes that current neuroimaging methods for measuring brain fluid dynamics lack formal validation. It calls for robust longitudinal studies and does not report any treatment, cure, or prevention for Alzheimer's disease.
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Butylphthalide may restore abnormal organization in structural networks of patients with MCI due to AD, and baseline network metrics could be predictive markers for therapeutic efficacy of butylphthalide.
Why it matters
In 270 people with mild cognitive impairment due to Alzheimer's disease, butylphthalide was linked to changes in brain network measures, with increased global efficiency in the structural network. This looks at brain network effects, not whether the drug prevents dementia or cures the disease.
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Baseline plasma NfL was associated with increased risk of dementia/death in the entire cohort.
Why it matters
This study found that baseline plasma neurofilament light, GFAP, and pTau181 were associated with increased risk of dementia or death and faster cognitive decline in people with mild cognitive impairment with Lewy bodies. These markers could help prognosis and stratification, but no treatment is tested.
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Our results reveal a spatial association between the epileptogenic focus and tau deposition, amyloid deposition, and neurodegeneration in early clinical stages of AD.
Why it matters
In eight patients with Alzheimer disease and seizures, tau deposition was greater in the hemisphere where seizures originated, with similar but weaker patterns for amyloid and atrophy. This describes an association between seizure focus and lateralized pathology in a small cross-sectional study and does not test any treatment.
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We tested the CSF of 40 patients with CBS (19 female patients, 65.9 ± 8.6 years) and 28 with PSP (13 female patients, 72.5 ± 8.7 years old), mostly White (n = 50) or Asian (n = 14). αSyn-SAA positivity was observed in 35.9% patients with CBS and 28.6% with PSP.
Why it matters
This cross-sectional study tested CSF from 40 patients with corticobasal syndrome and 28 with progressive supranuclear palsy for α-synuclein seed amplification. It examines biomarker detection in atypical parkinsonian disorders and does not test any 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.
- η-Secretase processing of APP inhibits neuronal activity in the hippocampus
- Suboptimal hydration remodels metabolism, promotes degenerative diseases, and shortens life
- Hydration water mobility is enhanced around tau amyloid fibers
- The ADAMs family: coordinators of nervous system development, plasticity and repair
- Brain connectivity in neurodegenerative diseases--from phenotype to proteinopathy
- Self-applied single-channel mastoid ExG for fully automated detection of REM sleep behaviour disorder
- Leukocyte telomere length and mortality in the Cardiovascular Health Study
- The mediational effects of FDG hypometabolism on the association between cerebrospinal fluid biomarkers and neurocognitive function
- Astrocyte-derived lipocalin-2 mediates hippocampal damage and cognitive deficits in experimental models of vascular dementia
- MMSE and MoCA in Parkinson's disease and dementia with Lewy bodies: a multicenter 1-year follow-up study