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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Human immunodeficiency virus (HIV) infection is commonly associated with neurological disease that occurs in the apparent absence of extensive infection of brain cells by HIV, suggesting that indirect mechanisms account for neuropathogenesis in the CNS, perhaps including changes in the normal neuroprotective functions of astrocytes.
Why it matters
In human fetal astrocytes grown in the laboratory, the inflammatory cytokine TNFalpha reduced glutamate uptake in a dose-dependent way. This is a cell study related to HIV-1 dementia, not a treatment or prevention for Alzheimer's disease.
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We assessed the validity and interrater reliability of neurologists who, using four different sets of previously published criteria for the clinical diagnosis of progressive supranuclear palsy (PSP), also called Steele-Richardson-Olszewski syndrome, rated 105 autopsy-proven cases of PSP (n = 24), Lewy body disease (n = 29), corticobasal ganglionic degeneration (n = 10), postencephalitic parkinsonism (n = 7), multiple system atrophy (n = 16), Pick's disease (n = 7), and other parkinsonian or dementia disorders (n = 12).
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47/100
APOE- epsilon 4 and non-epsilon 4 groups did not significantly differ in demographic, mental status, and functional characteristics.
Why it matters
Nondemented older adults carrying the APOE epsilon4 allele performed significantly worse on several verbal memory test measures than noncarriers. The results suggest episodic memory changes are associated with the epsilon4 allele and that such cognitive markers may precede later dementia, but no treatment was tested.
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The epsilon 4 allele of apolipoprotein E (apoE) is a major risk factor for Alzheimer disease, suggesting that apoE may directly influence neurons in the aging brain.
Why it matters
In a central nervous system-derived neuronal cell line, apoE3 increased neurite extension while apoE4 did not, and blocking the LRP receptor abolished the apoE3 effect. This is cell-based laboratory work that may provide insight into Alzheimer pathogenesis, not a treatment or prevention for patients.
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We quantified the synaptic population density in the frontal cortex of 25 individuals without dementia 16 to 98 years old, using sections double-immunolabeled for beta/A4 amyloid and for synaptophysin, and found a significant inverse correlation between the presynaptic terminal (PT) counts and age (r = -0.7, p < 0.001).
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Why it matters
Describes a method for determining apolipoprotein E genotype using one-stage PCR.
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Researchers conducted immunohistochemical studies on lipid changes in Alzheimer's disease brains using an antibody to apolipoprotein E. They unexpectedly discovered that apo E immunoreactivity was associated with amyloid in senile plaques, cerebral vessels, and neurofibrillary tangles, as well as in kuru plaques in Creutzfeldt-Jakob disease.
Why it matters
Reports apolipoprotein E staining in amyloid deposits and neurofibrillary tangles in Alzheimer's disease and in kuru plaque amyloid in Creutzfeldt-Jakob disease.
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Leuko-araiosis was found in 49 of 140 demented patients compared with 12 out of 110 control subjects.
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The clinical features of 11 families containing 73 individuals with dominantly inherited cerebellar ataxia of late onset are described.
Why it matters
This study describes the clinical features of 11 families with dominantly inherited late-onset cerebellar ataxia, in which some patients also had dementia. It concerns cerebellar ataxia and reports no treatment, cure or prevention for Alzheimer's disease.
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Post-mortem brain tissue from 15 patients dying with a diagnosis of senile dementia of Alzheimer type (SDAT) was compared with tissue obtained from 16 control patients at routine post-mortem.
Why it matters
In post-mortem brain tissue from 15 people with senile dementia of Alzheimer type, this study found reduced choline acetyltransferase activity and a 47% reduction in immunoreactive somatostatin in the temporal cortex. It describes brain changes found after death and does not test any treatment, cure, or prevention.
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No amyloid-related imaging abnormalities occurred.
Why it matters
A single 34-year-old symptomatic PSEN1 p.Met233Val carrier received 26 lecanemab infusions over 12 months with no amyloid-related imaging abnormalities, while composite Centiloid rose modestly and regional amyloid-PET changes diverged. This is one person's experience, so it cannot show whether lecanemab treats, cures, or prevents Alzheimer's disease in general.
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46/100
The locus coeruleus (LC) is the source of norepinephrinergic innervation in the human brain.
Why it matters
In this community-based cohort of 134 autopsied participants, locus coeruleus pTDP-43 pathology was found in about 21% of brains and was associated with depressive symptoms but not with global cognition. This suggests LC pTDP-43 pathology is a common feature of brain aging associated with LATE-NC, but its clinical significance for cognition is limited.
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46/100
GLP-1RA use was associated with a significantly lower risk of dementia [hazard ratio (HR) 0.80, 95% confidence interval (CI) 0.71-0.91, P = .001] and Alzheimer's disease (HR 0.76, 95% CI 0.59-0.98, P = .033) compared with DPP4i use.
Why it matters
In this observational study, people with diabetes and chronic kidney disease who took GLP-1 receptor agonists had a lower risk of being diagnosed with dementia and Alzheimer's disease than those who took DPP4 inhibitors. The study authors say more research is needed to confirm these findings, and no differences were seen for several other brain conditions.
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They are often found in middle-aged individuals and are associated with a greater risk of stroke and vascular dementia.
Why it matters
This study found that genetic predisposition to white matter hyperintensities was linked to larger volumes of them and to poorer executive function, with cardiac function proposed as a biological link. The authors note the polygenic risk score is not yet clinically actionable but suggest hemodynamic monitoring as an early, testable intervention in genetically susceptible people.
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Alzheimer's disease (AD) is a major public health concern in societies with increasingly ageing populations.
Why it matters
In PS19 tau mice, sleep loss and hyperarousal were more pronounced in males than females, and cognitive performance at 9 months was best predicted by earlier hyperarousal, wakeful EEG power and balanced NREM and REM sleep. This is a mouse study, so it cannot yet be applied to treating or preventing Alzheimer's disease in people.
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Additionally, growing evidence suggests that neuroinflammation may modulate the effects of tau spread on cognitive impairment in AD [Peretti, Débora E., et al., Brain 147.12 (2024): 4094‐4104.].
Why it matters
In older adults, those with positive p-tau217 and a faster annual rise in GFAP showed significantly faster cognitive decline than those without a fast GFAP rise. Baseline GFAP and p-tau217 did not show a significant interaction, and the authors conclude that the rate of GFAP change modifies the link between p-tau217 and cognitive decline.
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CSF Aβ42/Aβ40 contributed most to identify Aβ-positivity, while continuous Aβ-PET load within the positive range was best predicted by plasma P-tau217.
Why it matters
Machine learning models using CSF and plasma measures predicted quantitative amyloid PET, with plasma P-tau217 and CSF Aβ42/Aβ40 contributing most. Models using only plasma measures approached the performance of CSF models, suggesting blood tests may help track amyloid burden without PET.
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16% of individuals were identified as tau-accumulators.
Why it matters
Among amyloid-negative cognitively unimpaired individuals, 16% showed longitudinal tau accumulation across the neocortex, with preliminary links to a tau-specific CSF biomarker and focal atrophy but no difference in cognitive decline over time. The authors describe these as preliminary results, and no treatment, cure, or prevention is tested.
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The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections.
Why it matters
This review summarizes how autophagy and mitophagy at synapses relate to learning, memory and neurological disorders including Alzheimer's disease. It discusses diagnostic and therapeutic potential of autophagy-related pathways but presents no new treatment or cure.
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Neurodegenerative disorders alter mitochondrial functions, including the production of reactive oxygen species (ROS).
Why it matters
In this study, suppressing reactive oxygen species from mitochondrial complex III in mice reduced dementia-linked tauopathy and neuroimmune changes and extended lifespan. This identifies a possible therapeutic target but the work is in animal models and does not yet show benefit in people.
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GBA is the major risk gene for Parkinson’s disease (PD) and dementia with Lewy bodies (DLB), two common α-synucleinopathies with cognitive deficits.
Why it matters
In mouse models, this study found that Gba mutations contribute to cognitive deficits through α-synuclein-independent mechanisms involving dysfunction in synaptic vesicle endocytosis. These are animal findings, so they are early and preliminary and do not yet show a treatment for people.
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< 0.001), with the automated approach more likely to classify a scan as tau negative and lower agreement between methods in more severe cases and AD clinical variants.
Why it matters
Visual classification of tau-PET scans identified four tau patterns that differed in tau load, clinical features, and long-term outcomes, with one subtype showing steeper cognitive decline. The authors suggest this classification could be useful for personalized diagnosis and prognosis, but it does not test any treatment or cure.
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We found higher lipid droplet accumulation in primary fibroblasts derived from these mice, as well as in the brain of the mutant mice.
Why it matters
In a TDP-43 knock-in mouse model and postmortem FTLD-TDP tissue, TDP-43 dysfunction was linked to altered cholesterol-related lipid pathways, lipid droplet accumulation and myelination defects. This is laboratory and tissue research describing a disease mechanism, not a treatment, cure or prevention.
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Metabolomics has been associated with cognitive decline and dementia, but the relationship between metabolites and brain aging remains unclear.
Why it matters
In 17,770 participants free of chronic brain disorders, 64 and 77 plasma metabolites were associated with brain age and brain age gap, with lipids among those linked to larger or smaller gaps. This identifies associations between metabolites and brain aging, not a treatment, cure or prevention.
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46/100
Alpha-synuclein (aSyn) post-translational modifications (PTM), especially phosphorylation at serine 129 and C-terminal truncations, are highly enriched in Lewy bodies (LB), Lewy neurites, and other pathological aggregates in Parkinson's disease and synucleinopathies.
Why it matters
In a neuronal cell model, cutting off the tail end of alpha-synuclein protein at different stages affected how Lewy body-like clumps formed, and blocking certain enzymes changed this process. The authors say stage-specific strategies may be needed to target these protein cleavages, but this is laboratory work, not a treatment.
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.
- Neurotoxic complications of chemotherapy in patients with cancer: clinical signs and optimal management
- Frontotemporal dementia with the C9ORF72 hexanucleotide repeat expansion: clinical, neuroanatomical and neuropathological features
- Plasma P-tau181 and P-tau217 in Patients With Traumatic Encephalopathy Syndrome With and Without Evidence of Alzheimer Disease Pathology
- Terapia anti β-amiloide y enfermedad cerebrovascular: nuevos retos para la neurología vascular
- Cell cycle-dependent regulation of the phosphorylation and metabolism of the Alzheimer amyloid precursor protein
- PET imaging of 5-HT1A receptor binding in patients with temporal lobe epilepsy
- Chronic brain hypoperfusion causes early glial activation and neuronal death, and subsequent long-term memory impairment
- Lecanemab in DIAD: 6‐Month Amyloid PET Results from the DIAN‐TU‐001 Trial
- Digital and palmar dermatoglyphics in dementia of the Alzheimer type
- Astrocytes: Role and Functions in Brain Pathologies