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.
-
Consensus opinion characterizes dementia with Lewy bodies (DLB) as a progressive dementing illness, with significant fluctuations in cognition, visual hallucinations and/or parkinsonism.
Why it matters
This study found that visual hallucinations in Lewy body disease were related to Lewy bodies in the temporal lobe. It concerns Lewy body disease and does not test any treatment, cure or prevention for Alzheimer's disease.
-
Welders were exposed to a mean of 47,144 welding hours.
Why it matters
In this case-control study of 15 career welders compared with two control groups with idiopathic Parkinson's disease, welders had a younger age at onset (46 years) than sequentially ascertained controls (63 years). These preliminary data suggest welding may be a risk factor for parkinsonism, but they do not report anything about treating, curing, or preventing Alzheimer's disease.
-
Neurofibrillary tangles (NFT) composed of the microtubule-associated protein tau are prominent in Alzheimer disease (AD), Pick disease, progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD).
Why it matters
Mice engineered to carry human tau with P301L, the most common mutation behind the inherited dementia FTDP-17, developed movement and behaviour problems from 6.5 months (4.5 months with two copies of the gene), along with tau tangles, spinal-cord nerve loss and muscle wasting. Tangles formed mainly in deep brain regions and the spinal cord, with only early "pre-tangles" in the cortex and hippocampus, and the clumped tau matched tau from Alzheimer's and FTDP-17 brains. The authors offer it as a model for studying diseases with tangles. It is a mouse study, not a test of any treatment in people.
-
Autosomal recessive juvenile parkinsonism (AR-JP), one of the most common familial forms of Parkinson disease, is characterized by selective dopaminergic neural cell death and the absence of the Lewy body, a cytoplasmic inclusion body consisting of aggregates of abnormally accumulated proteins.
Why it matters
This laboratory study found that parkin — the protein made by the gene mutated in an inherited juvenile form of Parkinson's disease — helps tag proteins for disposal as a ubiquitin-protein ligase working with the enzyme UbcH7, and that faulty parkin from patients has lost this activity. The authors conclude that a build-up of proteins "that have yet to be identified" kills dopamine-producing nerve cells without forming Lewy bodies. They suggest the finding may help research into Alzheimer's and other diseases involving abnormal protein tagging, but the study tested nothing in Alzheimer's disease and no treatment.
-
CLBs detected by alpha-synuclein antibodies in patients with PD are a more sensitive and specific correlate of dementia than the presence of Alzheimer's pathology, which was present in a minority of the cases in this series.
Why it matters
In brains examined after death from 42 people with Parkinson's disease (22 with dementia, 20 without), cortical Lewy bodies stained for the protein alpha-synuclein matched dementia status with 91% sensitivity and 90% specificity. They tracked dementia better than Alzheimer-type plaques and tangles, which were present in only a minority of these brains. This is an association in one small autopsy series, not a test that can be used in living patients.
-
Structural maturation of fiber tracts in the human brain, including an increase in the diameter and myelination of axons, may play a role in cognitive development during childhood and adolescence.
Why it matters
This study found age-related increases in white matter density in fiber tracts of children and adolescents, including frontotemporal pathways. It is a developmental imaging study with no findings on treating, curing or preventing Alzheimer's disease.
-
56/100
Abeta1-42 is a self-associating peptide whose neurotoxic derivatives are thought to play a role in Alzheimer's pathogenesis.
Why it matters
This lab study found that small, diffusible oligomers of amyloid beta 1-42 (called ADDLs) killed mature neurons in brain tissue cultures at nanomolar concentrations and inhibited hippocampal long-term potentiation before cells degenerated. The authors hypothesize these oligomers could underlie early memory dysfunction and later cell loss in Alzheimer's disease.
-
Several members of the chemokine receptor family are used together with CD4 for HIV-1 entry into target cells.
Why it matters
This laboratory work identified CCR3 and CCR5 as co-receptors that HIV-1 uses to infect microglia, the brain's immune cells. It concerns HIV infection of the brain, not Alzheimer's disease, and reports no treatment, cure or prevention for Alzheimer's.
-
In patients with dementia, a positive immunoassay for the 14-3-3 brain protein in cerebrospinal fluid strongly supports a diagnosis of Creutzfeldt-Jakob disease.
Why it matters
This study describes a cerebrospinal fluid test for the 14-3-3 protein that detected Creutzfeldt-Jakob disease in 68 of 71 patients. It concerns diagnosis of transmissible spongiform encephalopathies, not the treatment, cure or prevention of Alzheimer's disease.
-
The micro-architecture of the substantia nigra was studied in control cases of varying age and patients with parkinsonism.
Why it matters
In brain tissue from 36 people without Parkinson's disease, pigmented nerve cells in the substantia nigra declined by about 4.7% per decade, mostly in the dorsal tier; in 20 people with Parkinson's disease, the loss was heaviest in the lateral ventral tier (an average of 91%), which is the opposite pattern. The authors say this suggests that ordinary age-related cell loss is not an important driver of Parkinson's disease. The study is about Parkinson's disease, not Alzheimer's, and does not address treatment or prevention.
-
We detected large numbers of HLA-DR-positive reactive microglia (macrophages), along with Lewy bodies and free melanin, in the substantia nigra of all cases studied with Parkinson's disease (5) and parkinsonism with dementia (PD) (5).
Why it matters
In post-mortem brains, this 1988 study found many HLA-DR-positive reactive microglia (immune cells of the brain) in the substantia nigra of all 10 people with Parkinson's disease or parkinsonism with dementia. It found milder changes of the same kind in 6 of 9 people with Alzheimer-type dementia, compared with 1 of 11 people without neurological disease. The authors read the microglia as "a sensitive index of neuropathologic activity" and suggested that Alzheimer- and Parkinson-type pathology often occur together in older people, but the study had only 30 brains, reported no statistics, and cannot show cause or offer a test for living patients.
-
The Lewy body is a distinctive neuronal inclusion that is always found in the substantia nigra and other specific brain regions in Parkinson's disease.
Why it matters
In 273 brains from people who died of disorders other than Parkinson's disease, the authors found Lewy bodies in 3.8% of people in their sixth decade, rising to 12.8% in their ninth. They interpret these "incidental" cases as probably presymptomatic Parkinson's disease, a reading based on post-mortem findings rather than on following anyone in life, and they propose, without testing it here, that early-life internal mechanisms may matter more than environmental agents. The paper is about Parkinson's disease, not Alzheimer's, and it does not test any treatment or prevention.
-
The study included 560 amyloid-positive participants (BioFINDER: n = 431; mean [SD] age, 73.6 [7.0] years; 212 female [49.2%] and 219 male [51.8%]; TRIAD: n = 129; mean [SD] age, 70.4 [8.3] years; 76 female [58.9%] and 53 male [41.1%]).
Why it matters
A panel of 7 plasma proteins identified advanced tau pathology in amyloid-positive people better than p-tau217 alone, and reduced the number of people falling into an uncertain intermediate-risk range. This suggests a blood-based multiprotein test may offer a scalable alternative to tau PET staging in clinical or research settings.
-
55/100
In 7989 cognitively unimpaired participants (median [range] age, 54 [30-90] years; 4877 [61.3%] female; mean [SD] BMI, 25.9 [4.2]; mean [SD] eGFR, 80.7 [14.7] mL/min/1.73 m2), older age, lower BMI, and reduced kidney function were associated with increased NfL and GFAP concentrations; female sex was associated with increased GFAP concentrations.
Why it matters
This study established reference intervals for GFAP and NfL in healthy individuals, showing that age, BMI, kidney function and sex affect these levels. It is about interpreting biomarker measurements, not about treating or preventing Alzheimer's disease.
-
Alzheimer's disease (AD) is the leading cause of dementia and is characterized by progressive amyloid accumulation followed by tau-mediated neurodegeneration.
Why it matters
In this study, anti-amyloid chimeric antigen receptors expressed in astrocytes reduced amyloid and associated pathology and prevented early plaque deposition in vivo. The findings support CAR-A as a potential disease-modifying strategy but are early work and do not yet show benefit in people.
-
With blood-based phosphorylated tau biomarkers soon to be used for diagnosis of Alzheimer disease, analyzing tau levels in other conditions could enhance biomarker interpretability.
Why it matters
This study measured phosphorylated and nonphosphorylated tau variants in the blood of patients with multiple traumatic injuries to better understand what drives tau release into the blood. It concerns trauma, not Alzheimer's disease treatment, cure, or prevention.
-
Aggregation of the protein tau defines tauopathies, the most common age-related neurodegenerative diseases, which include Alzheimer's disease and frontotemporal dementia.
Why it matters
A genome-wide CRISPR screen in human iPSC-derived neurons identified cellular pathways and the E3 ubiquitin ligase CRL5 SOCS4 that control tau levels and aggregation. These results suggest possible therapeutic targets for tauopathies, but they come from laboratory cell models and no treatment has been tested in patients.
-
The viral-inflammatory hypothesis of Alzheimer's disease offers a new paradigm, yet interventions like antivirals and vaccination present a paradox that challenge therapeutic development.
Why it matters
This perspective argues that trials of antivirals and vaccines for dementia may have missed real biological effects because they did not measure synaptic biomarkers, and it notes that the first major antiviral randomized controlled trial was negative. It proposes using synaptic markers as trial endpoints but does not itself show that any antiviral or vaccine prevents or treats Alzheimer's disease.
-
Depression is a known risk factor for dementia and MCI, but its associations with AT(N) biomarkers remain inconsistent and may differ by cognitive status.
Why it matters
This cross-sectional study examined depressive symptoms alongside plasma amyloid, tau, and neurofilament light biomarkers in dementia-free and mildly cognitively impaired participants. It does not report any treatment, cure, or prevention, and no conclusions about altering disease course can be drawn from it.
-
In frontotemporal dementia and amyotrophic lateral sclerosis, the RNA-binding protein TDP-43 is depleted from the nucleus of neurons in the brain and spinal cord.
Why it matters
This study found that loss of TDP-43 from neuronal nuclei is linked to widespread changes in alternative polyadenylation, affecting disease-relevant genes such as SFPQ, NEFL and TMEM106B. It describes a new facet of TDP-43 pathology but does not test any therapy.
-
Forty-three proteins were differentially regulated in FTD compared to controls and AD, reflecting axon development, regulation of synapse assembly, and cell-cell adhesion mediator activity pathways.
Why it matters
This study identified cerebrospinal fluid protein panels that accurately discriminate frontotemporal dementia from controls and Alzheimer's disease. It introduces potential diagnostic biomarkers, but it does not report any treatment, cure, or prevention for Alzheimer's disease.
-
Our results suggest that microstructural features derived from NODDI such as fISO might be useful adjunct markers to tau, which needs to be confirmed in longitudinal studies.
Why it matters
In 80 participants from the ADNI-3 dataset, a diffusion imaging measure called free-water mediated the relationship between cortical thickness/subcortical volume and tau. The authors suggest this measure might be a useful adjunct marker to tau, but say it needs confirmation in longitudinal studies.
-
Almost all individuals with Down Syndrome (DS) develop Alzheimer's disease (AD) by mid to late life.
Why it matters
This proteomic study of cerebrospinal fluid found that people with Down syndrome showed more severe changes in immune-related proteins, extracellular matrix pathways, and blood-brain barrier-related proteins compared to late-onset Alzheimer's disease, with some changes present before amyloid or tau pathology. The authors suggest these unique features may have implications for treatment strategies, but no treatment is tested here.
-
55/100
Of 104 metabolites studied, glycodeoxycholic acid (GDCA) surpassed the false discovery rate and was associated the Alzheimer's Disease Assessment Scale-Cognitive Subscale version 13 (ADAS-Cog13) score (β = 0.12, 95 % CI = 0.05-0.20, p = 0.001) and cognitive impairment determined by mini-mental status exam (MMSE) (OR = 2.11, 95 % CI = 1.41-3.15, p < 0.001).
Why it matters
Higher levels of a gut metabolite called glycodeoxycholic acid were linked to worse cognition, but only in people with low white matter hyperintensity burden, not in those with high burden. This is a cross-sectional finding and does not show that changing this metabolite would affect memory or dementia.
-
We used an untargeted mass spectrometric approach, tandem mass tag proteomics, for the identification of proteomic signatures in genetic frontotemporal dementia (FTD).
Why it matters
This proteomic analysis found shared and distinct cerebrospinal fluid protein alterations in each genetic form of frontotemporal dementia, with some changes already evident in presymptomatic mutation carriers. These findings may help identify proteins involved in neurodegeneration and glial responses, but no treatment or cure is reported.
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.
- Structural development of the hippocampus and episodic memory: developmental differences along the anterior/posterior axis
- The biochemical pathway of neurofibrillary degeneration in aging and Alzheimer's disease
- Autoradiography validation of novel tau PET tracer [F-18]-MK-6240 on human postmortem brain tissue
- Plasma pTau181 and amyloid markers predict conversion to dementia in idiopathic REM sleep behaviour disorder
- Role of apolipoprotein E in neurodegenerative diseases
- Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease
- Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS
- Increased proliferation reflects glial and vascular-associated changes, but not neurogenesis in the presenile Alzheimer hippocampus
- Biomarkers and therapeutic strategies targeting microglia in neurodegenerative diseases: current status and future directions
- DNA methylation patterns contribute to changes of cellular differentiation pathways in leukocytes with LOY from patients with Alzheimer´s disease