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.
-
To investigate earlier pathologies preceding filamentous tau inclusions, researchers studied wild-type and P301S mutant human tau transgenic mice.
Why it matters
Reports that in a P301S tauopathy mouse model, synapse loss and microglial activation came before tangles.
-
Empathy is a complex social behaviour mediated by a network of brain structures.
Why it matters
In 123 patients with several neurodegenerative diseases, empathy scores correlated with the volume of specific right-sided brain regions including the right temporal pole and subcallosal gyrus. This maps where empathy loss comes from but does not offer a treatment or cure.
-
Certain disease states are characterized by disturbances in production, accumulation or clearance of protein.
Why it matters
This study describes a method to measure how fast amyloid-beta is produced and cleared in the human central nervous system. It could help researchers understand whether production or clearance problems cause sporadic Alzheimer's disease, but it does not test a treatment.
-
Parkinson's disease (PD; OMIM #168600) is the second most common neurodegenerative disorder in the Western world and presents as a progressive movement disorder.
Why it matters
This study cloned a novel gene containing missense mutations that segregate with PARK8-linked Parkinson's disease in five families, naming the protein dardarin. It concerns the genetics of familial Parkinson's disease, not treating, curing or preventing Alzheimer's disease.
-
Genomic triplication of the alpha-synuclein gene (SNCA) has been reported to cause hereditary early-onset parkinsonism with dementia.
Why it matters
This study found that duplication of the alpha-synuclein gene causes an inherited form of parkinsonism whose symptoms closely resemble idiopathic Parkinson's disease, with late onset and slow progression. It concerns Parkinson's disease genetics, not Alzheimer's disease, so it does not directly inform Alzheimer's treatment, cure or prevention.
-
Inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia (IBMPFD) is a dominant progressive disorder that maps to chromosome 9p21.1-p12.
Why it matters
Six missense mutations in the gene encoding valosin-containing protein (VCP) were found in all 61 affected individuals with inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia. This identifies a genetic cause and a possible common ubiquitin-based pathway, but no treatment was tested.
-
The presence of epsilon 4 was associated with risk of developing AD on follow-up (relative risk, 1.92; 95% confidence interval, 1.27-2.89).
Why it matters
In older Catholic clergy followed for up to 6 years, carrying the APOE epsilon4 allele was linked to a higher risk of developing Alzheimer's disease and to faster decline across several thinking abilities, especially episodic memory. This describes risk and decline patterns but does not test any treatment or prevention.
-
Protein-energy malnutrition (PEM) is common in connection with chronic disease and is associated with increased morbidity and mortality.
Why it matters
This review of protein-energy malnutrition treatment reports that dietary supplements, alone or with hormonal treatment, may have positive effects in patients with manifest or at-risk malnutrition, but notes major methodological problems in such studies. It covers chronic disorders including dementia but does not show that nutritional support prevents or cures Alzheimer's disease.
-
Human immunodeficiency virus-1 (HIV-1) can induce dementia with alarming occurrence worldwide.
Why it matters
This review describes how HIV-1 infects macrophages and microglia but not neurons, with neurons injured and dying by apoptosis mainly through indirect toxins released by these cells. It concerns HIV-associated dementia mechanisms and does not report a treatment, cure or prevention for Alzheimer's disease.
-
Two mutations in the gene encoding alpha-synuclein have been linked to early-onset Parkinson's disease (PD). alpha-Synuclein is a component of Lewy bodies, the fibrous cytoplasmic inclusions characteristic of nigral dopaminergic neurons in the PD brain.
Why it matters
In test-tube experiments with purified alpha-synuclein, the normal protein and two mutant forms linked to early-onset familial Parkinson's disease (A53T and A30P) were all unstructured when dilute, but at higher concentrations formed Lewy body-like fibrils and spherical clumps, most rapidly with A53T. The authors conclude that faster fibril formation "may contribute" to the early onset of familial Parkinson's disease. This is protein chemistry, not a study of patients, and it is not about Alzheimer's or any treatment.
-
Frontotemporal dementia with parkinsonism, chromosome 17 type (FTDP-17), a recently defined disease entity, is clinically characterized by personality changes sometimes associated with psychosis, hyperorality, and diminished speech output, disturbed executive function and nonfluent aphasia, bradykinesia, and rigidity.
Why it matters
This genetic study examined the tau gene as a candidate for chromosome 17 frontotemporal dementia and found a Val279Met variant that evidence indicated is a causative mutation in one family. It concerns frontotemporal dementia genetics and does not test any treatment, cure, or prevention for Alzheimer's disease.
-
Lewy bodies and Lewy neurites are the defining neuropathological characteristics of Parkinson's disease and dementia with Lewy bodies.
Why it matters
This laboratory study found that alpha-synuclein is the major filamentous component of Lewy bodies and Lewy neurites, and that staining for alpha-synuclein is better than staining for ubiquitin at detecting them. It concerns Parkinson's disease and dementia with Lewy bodies, not Alzheimer's disease treatment, cure or prevention.
-
Genetic causes of Alzheimer's disease (AD) include mutations in the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) genes.
Why it matters
In mice, combining a mutant APP gene (the Tg2576 line) with a mutant presenilin 1 gene (PS1M146L) produced "large numbers of fibrillar A beta deposits in cerebral cortex and hippocampus far earlier" than in littermates carrying the APP mutation alone, even though PS1-mutant mice on their own "do not show abnormal pathology." Before any deposits appeared, the double-mutant mice already had a "selective 41% increase" in the brain's amyloid-beta 42(43), the form the authors describe as "highly amyloidogenic." This is an animal study of genes linked to inherited Alzheimer's, so it does not show how to treat or prevent the disease in people.
-
Stroke is the third leading cause of death, and vascular dementia the second cause of dementia after Alzheimer's disease.
Why it matters
This study identified mutations in the Notch3 gene in patients with CADASIL, a hereditary adult-onset condition causing stroke and vascular dementia. It concerns the genetic cause of CADASIL, not treating, curing or preventing Alzheimer's disease.
-
Why it matters
Reports that cultured cells produce amyloid β-peptide during normal metabolism.
-
Several families with an early-onset form of familial Alzheimer's disease have been found to harbour mutations at a specific codon (717) of the gene for the beta-amyloid precursor protein (APP) on chromosome 21.
Why it matters
This study reports a mutation at codon 692 of the beta-amyloid precursor protein gene that co-segregates in one family with presenile dementia and cerebral haemorrhage due to cerebral amyloid angiopathy. The results suggest that these clinically distinct entities can be caused by the same mutation in the APP gene.
-
< 0.01). Using an operationalization of clinical criteria for LATE, 8.2% of participants with MCI or dementia from our tertiary memory clinic were classified as Possible-LATE, Probable-LATE, or LATE-AD.
Why it matters
Using proposed clinical criteria, about 8 in 100 people at a memory clinic with mild cognitive impairment or dementia were classified as having suspected LATE, a condition related to TDP-43 protein. Those with probable LATE had a milder course than Alzheimer's disease, while those with LATE plus Alzheimer's had a more aggressive course, which may help doctors give more accurate diagnoses and prognoses.
-
Collectively, plasma biomarker findings in the low p-tau217 subgroup were more robust than in the mITT population.
Why it matters
In a phase 2 trial, people with Alzheimer's who took zervimesine had a significant drop in blood GFAP, a marker of brain inflammation, compared with placebo, while NfL, Aβ42 and Aβ40 only trended downward; results were clearer in a subgroup with low p-tau217. These biomarker findings are exploratory, but the authors say they line up with the clinical benefit seen in the SHINE trial and support testing the drug in patients with less disease pathology.
-
Of 70 autopsied individuals (62 male, 8 female; mean [SD] age, 64.40 [13.94] years), 20 showed CTE-NC in the brain.
Why it matters
In this autopsy case-control study, all cases with chronic traumatic encephalopathy neuropathologic changes had spinal cord p-tau deposits, often alongside TDP-43, Aβ and α-synuclein deposits, and spinal p-tau was linked to microglial activation and motor symptoms. These are post-mortem observations about co-pathologies and do not provide a treatment or cure.
-
57/100
Aging and age-related diseases share convergent pathways at the proteome level.
Why it matters
Using plasma proteomics, this study built organ-specific aging clocks and found that brain aging was linked to cognitive decline and dementia and could stratify Alzheimer's disease risk across APOE types. It is a risk-prediction framework and does not test any treatment, cure, or prevention.
-
57/100
The beneficial effects of a ketogenic diet (KD) on neurodegenerative conditions such as mild cognitive impairment (MCI) and Alzheimer disease (AD) are increasingly acknowledged, with potential implications for the general population as well.
Why it matters
In 11 cognitively healthy people with overweight, a 3-week ketogenic diet increased cerebral blood flow and raised BDNF levels. This is a very small, short study in healthy people, so it does not show whether a ketogenic diet prevents or treats Alzheimer's disease.
-
DTI-ALPS values were significantly lower compared to HC in both DLB (Estimate = -0.084 [-0.14 to -0.03], p = 0.004) and MCI-LB (Estimate = -0.058 [-0.11 to -0.002], p = 0.047) DTI-ALPS was also significantly associated with both baseline (t[147] = 2.22, p = 0.028) and longitudinal decline (t[127] = 2.41,p = 0.017) in cognitive score.
Why it matters
A brain imaging measure called DTI-ALPS was lower in people with dementia with Lewy bodies and mild cognitive impairment with Lewy bodies compared to healthy controls, and it was linked to cognitive decline and to blood markers of nerve and astrocyte damage. The authors say further research is needed to clarify the role of the glymphatic system and whether DTI-ALPS specifically measures it.
-
We recruited 210 participants; 205 (66.8% male; aged 66.4±11.1 years) had useable data.
Why it matters
Higher arterial pulsatility was linked to more white matter hyperintensities and perivascular spaces at baseline, but not to their change over 1 year or to cognition, dependency or stroke. The authors conclude that these findings question the idea that high intracranial pulsatility causes small vessel disease progression.
-
The study included 356,173 participants (median age 56 years; 53.69% female).
Why it matters
In 356,173 participants, shorter leucocyte telomere length was associated with higher incidence of stroke, dementia and late-life depression, but Mendelian randomization analyses did not identify causal relationships between telomere length and these outcomes. The study reports associations only and does not test any treatment, cure or prevention.
-
With the moderate sample size of the current study, treatment using sodium benzoate, a DAO inhibitor, showed promise in improving cognition, especially short-term memory, in patients with aMCI.
Why it matters
In 82 people with amnestic mild cognitive impairment, sodium benzoate significantly improved short-term memory but only showed a nonsignificant trend for overall cognition. This is a single moderate-sized trial and does not show prevention or cure of Alzheimer's disease.
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.
- Intermittent fasting reprograms the brain proteome to prevent synaptic degeneration and cognitive impairment in vascular dementia
- Association of Bilateral Salpingo-Oophorectomy Before Menopause Onset With Medial Temporal Lobe Neurodegeneration
- Spreading of Beta-Amyloid in Organotypic Mouse Brain Slices and Microglial Elimination and Effects on Cholinergic Neurons
- Contribution of hyperammonemia and inflammatory factors to cognitive impairment in minimal hepatic encephalopathy
- Elevated TDP-43 serum levels associated with postoperative delirium following major cardiac surgery
- Amygdala nuclei are not uniformly vulnerable to FTLD‐tauopathies in PPA
- TREM2 macrophages induced by human lipids drive inflammation in acne lesions
- Multi-modal characterization of rapid anterior hippocampal volume increase associated with aerobic exercise
- Identification and cloning of human astrocyte genes displaying elevated expression after infection with HIV-1 or exposure to HIV-1 envelope glycoprotein by rapid subtraction hybridization, RaSH