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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Filamentous tau aggregates are hallmarks of tauopathies, e.g., frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) and amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC).
Why it matters
Transgenic mice overexpressing the smallest human tau isoform developed age-dependent tau pathology, including insoluble hyperphosphorylated tau and inclusions, with axon degeneration and motor weakness. This is an animal model for studying tauopathies, not a treatment or cure.
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HIV-1 glycoprotein gp120 induces injury and apoptosis in rodent and human neurons in vitro and in vivo and is therefore thought to contribute to HIV-associated dementia.
Why it matters
In rat cerebrocortical cultures, HIV gp120 was shown to cause neuronal apoptosis, possibly through direct interaction with neurons or indirectly via glial release of neurotoxic factors. This is laboratory work on HIV-associated dementia, not a treatment, cure or prevention for Alzheimer's disease.
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In Alzheimer disease (AD), neurons are thought to be subjected to the deleterious cytotoxic effects of activated microglia.
Why it matters
This laboratory work describes a pathway in which amyloid-β binding to the RAGE receptor on neurons triggers M-CSF, a proinflammatory signal, and AD brain tissue and spinal fluid showed increased M-CSF. It identifies a possible inflammatory mechanism but does not test any treatment or show that blocking it helps patients.
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Senile plaques (SP) are complicated lesions composed of diverse amyloid peptides and associated molecules, degenerating neuronal processes,a nd reactive glia.
Why it matters
This review discusses how senile plaques form over time and how different forms of amyloid may be involved. It is a discussion of disease mechanisms and does not test any treatment or prevention.
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It has been suggested that dietary antioxidants reduce Parkinson's disease (PD) risk by neutralizing free radicals, thus preventing injury to neurons in the substantia nigra.
Why it matters
This case-control study examined whether long-term dietary antioxidant intake affects Parkinson's disease risk, not Alzheimer's disease. It found no protective effect and even trends toward greater risk with higher intake of some antioxidants, so it provides no support for antioxidants reducing Parkinson's risk.
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To gain insights into the significance of presenilins (PS) in the pathogenetic mechanisms of early-onset familial Alzheimer disease (FAD), we expressed cDNAs for wild-type PS2 and PS2 with the Volga German (N141I) mutation in cultured cells and then examined the metabolism of the transfected proteins and their effect on the C-terminal properties of secreted amyloid beta protein (A beta).
Why it matters
In cultured COS-1 cells and mouse Neuro2a cells, the PS2 N141I mutation found in Volga German families with early-onset familial Alzheimer's left the PS2 protein's own processing unchanged, but the cells secreted "1.5- to 10-fold more" amyloid beta ending at residue 42 (or 43) than cells with normal PS2. The authors say this "strongly suggest[s]" the mutation shifts processing toward "the form of A beta that most readily deposits in amyloid plaques." This was cell-culture work only; it did not study patients and offers no treatment.
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Current concepts of the pathogenesis of Parkinson's disease (PD) center on the formation of reactive oxygen species and the onset of oxidative stress leading to oxidative damage to substantia nigra pars compacta.
Why it matters
This review of Parkinson's disease describes evidence of oxidative stress, including altered brain iron, impaired mitochondrial function, and changes in antioxidant systems such as superoxide dismutase and reduced glutathione. A loss of glutathione is associated with incidental Lewy body disease and may be the earliest biochemical marker of nigral cell loss, though glutathione depletion alone may not damage nigral neurons but may increase susceptibility to later toxic or free radical exposure.
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Cerebral cortical dysgenesis (CD) is a heterogeneous disorder of cortical development and organization commonly associated with epilepsy, with a variety of subtypes.
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Ventricular enlargement and white matter lesions are frequent findings on cerebral magnetic resonance imaging scans of elderly subjects.
Why it matters
This study looked at whether enlarged brain ventricles and white matter lesions seen on MRI are related to cognitive function in 90 older people without dementia. It helps clarify the meaning of these common brain scan findings in people without dementia, but no treatment was tested.
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A genetic classification of Alzheimer disease(s) (AD) is presented.
Why it matters
This paper presents a hypothesis that people who inherit APOE4 alleles may have a metabolic process leading to increased risk and earlier onset of late-onset Alzheimer's disease, and that apoE3 binds tau while apoE4 does not. It is a hypothesis about a possible mechanism and does not provide a treatment, cure, or prevention for Alzheimer's disease.
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The cellular mechanism underlying the generation of beta-amyloid in Alzheimer disease and its relationship to the normal metabolism of the amyloid precursor protein are unknown.
Why it matters
This laboratory study shows that 3- and 4-kDa peptides related to beta-amyloid are normally secreted by cells and that Golgi processing inhibitors block this secretion. It helps explain how beta-amyloid is made but does not test any treatment, cure, or prevention in people.
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Extracellular deposition of the beta/A4 amyloid peptide is a characteristic feature of the brain in patients with Alzheimer disease. beta/A4 amyloid is derived from the amyloid precursor protein (APP), an integral membrane protein that exists as three major isoforms (APP695, APP751, and APP770).
Why it matters
In PC12 cells, phorbol ester treatment increased secretion of APP695, APP751 and APP770, and this increase was augmented by okadaic acid. This is laboratory research and does not test a treatment or cure for Alzheimer's disease.
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50/100
The decline in the high incidence of amyotrophic lateral sclerosis, parkinsonism, and Alzheimer-type dementia among the Chamorro population of the western Pacific islands of Guam and Rota, coupled with the absence of demonstrable viral and hereditable factors in this disease, suggests the gradual disappearance of an environmental factor selectively associated with this culture.
Why it matters
In monkeys, a compound from cycad seeds produced motor neuron dysfunction and parkinsonian features, supporting a possible environmental cause of the Guam disease. This is animal and epidemiological evidence about cause, not a treatment or cure for Alzheimer's disease.
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At baseline, the mean MNA score was 22.5 ± 2.3.
Why it matters
In this 6-month trial, older adults at risk of undernutrition and cognitive decline who received a protein-enriched Mediterranean diet, with or without exercise, showed improved nutritional status and cognitive function compared with the control group. Correcting undernutrition could help slow cognitive decline and promote physical health during aging.
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Tau pathology spreads cell to cell, but the mechanisms of intercellular tau transmission remain unclear.
Why it matters
This work found that the neuronal gene Arc is critical for packaging tau into extracellular vesicles and for intercellular tau transmission, with intercellular tau transmission almost absent in Arc knockout mice. These are animal and cell findings about how tau spreads, not a treatment, cure or prevention for Alzheimer's disease.
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O]water PET were strongest for 1800 msec single-PLD and generally decreased with longer PLDs, except the occipital lobe, where all PLDs showed poor agreement.
Why it matters
This study compared different timing settings for a type of MRI that measures blood flow in the brain, finding that a 1800 msec delay correlated best with PET blood flow measures. It is a methods study about imaging technique and does not test any treatment, cure, or prevention.
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Postoperative Cognitive Dysfunction (POCD) is a common complication in older adults undergoing major surgery and is associated with prolonged recovery and long-term cognitive decline.
Why it matters
This systematic review examined whether preoperative inflammatory and neurodegenerative protein biomarkers can predict postoperative cognitive dysfunction in older adults having orthopedic surgery. The goal is early risk stratification and personalized perioperative management, not treating, curing or preventing Alzheimer disease.
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In the cohort, 39.2% (67/171) tested positive by α-syn SAA. α-syn SAA positivity was more frequently detected alone than in combination with biomarkers of AD pathology (25.1% vs. 14.0%). α-syn SAA+ status was independently associated with higher odds of fluctuating cognition (OR 2.99, 95%CI 1.46–6.25, p = 0.012), visual hallucinations (OR 2.41, 95%CI 1.24–4.75, p = 0.027), extrapyramidal signs (OR 4.57, 95%CI 2.35–9.11, p < 0.001) and akinetic mutism (OR 3.77, 95%CI 1.22–12.82, p = 0.038).
Why it matters
In patients with rapidly progressive dementias, Lewy body pathology was common but clinical features did not reliably predict it. The findings support using biomarkers to help diagnose Lewy body pathology in these patients.
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Collectively, these findings suggest that Aβ promotes gut symptoms through alteration of ENS connectivity and butyrate counteracts these impairments with an amelioration of neuroinflammation and memory function in AD model.
Why it matters
In a mouse model of Alzheimer's disease, the short-chain fatty acid butyrate reduced neuroinflammation and improved memory function. These findings are from an animal model and do not yet show whether butyrate would have the same effects in people.
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49/100
= 0.64). In AD-relevant regions, increased free water correlates with tau load independently of macrostructural metrics or amyloid load.
Why it matters
In Alzheimer's-relevant brain regions, higher free water correlated with tau tangle load independently of macrostructural measures or amyloid load. This suggests free water could serve as an imaging marker of microstructural gray matter changes, not as a treatment or cure.
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In the central Lewy body diseases (LBDs) Parkinson's disease and dementia with Lewy bodies (DLB), by the time parkinsonism or cognitive dysfunction manifests, substantial central neurodegeneration has already occurred.
Why it matters
This review of the longitudinal PDRisk study describes candidate biomarkers, such as cardiac sympathetic neuroimaging and cerebrospinal fluid measures, that might detect Lewy body diseases before symptoms appear. The stated goal is to enable testing of strategies that might delay symptom onset, but no such strategy is tested here.
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Raw scores were converted to regression‐based Z‐scores and averaged at the domain and overall level.
Why it matters
In 560 adults in Uganda, higher plasma neurofilament light was linked to worse cognition across several domains, and higher GFAP was linked to worse executive function, while p-tau217, Aβ42/40 and their ratio were not associated with cognition. The authors suggest cognitive impairment in this younger group may be driven by non-Alzheimer's causes.
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All included PD patients were cognitively normal at baseline and had 6 years of follow-up assessments available for cognitive status.
Why it matters
This study found that Parkinson's disease patients who developed mild cognitive impairment showed greater atrophy and white matter hyperintensity progression in frontal brain regions than those who remained cognitively healthy. This may help understand the pathology, but no treatment or cure is tested.
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Dementia is a defining feature of Lewy body disease: its timing and onset distinguish different clinical diagnoses, and its effect on quality of life is profound.
Why it matters
This in-vivo neuroimaging study found divergent structural connectivity patterns between Parkinson's disease with normal cognition and Lewy body dementia, with differences particularly in layer 4 excitatory neurons. It does not test any treatment or prevention, so its relevance to curing or preventing dementia is limited to understanding how these conditions differ.
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49/100
Aggregated TDP-43 is a hallmark of frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), and limbic-predominant age-related TDP-43 encephalopathy (LATE), and a common co-pathology in other neurodegenerative diseases.
Why it matters
Two new radiopharmaceuticals were developed that bind aggregated TDP-43 with high affinity and show selectivity over Aβ, tau and α-synuclein aggregates, with suitable brain imaging profiles in non-human primates. These are candidate PET imaging tracers for diagnosis, not a treatment, cure or prevention.
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.
- Associations of plasma p‐tau231 with serial position recall performance in free‐of‐dementia individuals
- Prevalence of Intracranial Atherosclerotic Stenosis Using High-Resolution Magnetic Resonance Angiography in the General Population: The Atherosclerosis Risk in Communities Study
- Soluble TREM2 and Inflammatory Proteins in Alzheimer's Disease Cerebrospinal Fluid
- Characterizing Macrophage Diversity in Metastasis-Bearing Lungs Reveals a Lipid-Associated Macrophage Subset
- Disturbance of nuclear and cytoplasmic TAR DNA-binding protein (TDP-43) induces disease-like redistribution, sequestration, and aggregate formation
- Association of Chronic Pain with Biomarkers of Neurodegeneration, Microglial Activation, and Inflammation in Cerebrospinal Fluid and Impaired Cognitive Function
- Molecular imaging with Pittsburgh Compound B confirmed at autopsy: a case report
- Circulating Brain-Related miRNAs as Predictors of Postoperative Delirium in Cardiac Surgery Patients
- Identification of a broadly fibrogenic macrophage subset induced by type 3 inflammation
- TDP-43 oxidation and PP1 crosstalk at RNA granule-mitochondria contact sites