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.
-
While dementia has been observed in approximately one-fourth of terminally ill patients with acquired immunodeficiency syndrome, it has been difficult to attribute this clinical disorder to a single neuropathological substrate.
Why it matters
This autopsy study found that multinucleated giant cells were present in only half of dementia patients, but all dementia patients had severe HIV encephalitis as assessed by intra-central nervous system viral burden. The authors interpret additional patients with severe HIV encephalitis but no clinical dementia history as evidence that HIV encephalitis exists for a period before clinical symptoms develop.
-
Accumulation of the amyloid A beta peptide, which is derived from a larger precursor protein (APP), and the formation of plaques, are major events believed to be involved in the etiology of Alzheimer's disease.
Why it matters
This study found that APP is phosphorylated at Thr668 by cdc2 kinase in a cell cycle-dependent manner in vitro and in vivo. It is laboratory research on APP metabolism and does not test any treatment, cure, or prevention.
-
Major membrane lipids were quantified in frontal (Brodmann area 9) and temporal (Brodmann areas 21 and 22) cortices, caudate nucleus, hippocampus, and frontal white matter of 12 cases with Alzheimer's disease (AD) type I (early onset), 21 cases with AD type II (late onset), and 20 age-matched controls.
Why it matters
This study measured membrane lipids in brain tissue from 12 early-onset and 21 late-onset Alzheimer's cases and 20 controls, finding reduced gangliosides and phospholipids particularly in early-onset cases. It suggests synapse loss in early-onset and demyelination in late-onset forms but does not test a treatment or cure.
-
The serine protease inhibitor alpha 1-antichymotrypsin (ACT) consistently colocalizes with amyloid deposits of Alzheimer's disease (AD) and may contribute to the generation of amyloid proteins and/or physically affect fibril assembly.
Why it matters
In laboratory experiments, alpha 1-antichymotrypsin bound to synthetic amyloid-beta peptides and caused fibril disaggregation in vitro. This is a test-tube study and does not show any treatment, cure, or prevention for Alzheimer's disease in people.
-
We used magnetic resonance imaging to examine the morphologic characteristics of the amygdala/hippocampus, prefrontal cortex, and caudate nucleus in 29 healthy volunteers matched for age, gender, and head of household socioeconomic status and 44 patients with chronic schizophrenia.
-
In a study of 52 individuals belonging to 35 species or subspecies of passerine birds it was shown that the volume of the hippocampal complex relative to brain and body size is significantly larger in species that store food than in species that do not.
-
Deposition of amyloid filaments serves as a pathologic hallmark for some neurodegenerative disorders.
Why it matters
In developing hamster brain, injections of nerve growth factor increased mRNA levels for the prion protein and the beta-amyloid protein precursor in regions containing NGF-responsive cholinergic neurons. This is animal work on gene regulation and does not show any way to treat, cure or prevent Alzheimer's disease.
-
The degree of neurofibrillary tangle formation, granulovascuolar degeneration, and nerve cell loss was quantified in serial sections of the hippocampal formation from the brains of 5 adults dying with Down syndrome (monogolism).
Why it matters
In hippocampal tissue from 5 adults with Down syndrome, the number of Alzheimer neurofibrillary tangles and loss of pyramidal neurons were as severe as in patients with Alzheimer dementia. This is a small, older quantitative comparison that suggests a shared mechanism, but it tests no treatment or prevention.
-
TDP-43 is a ubiquitously expressed, primarily nuclear DNA/RNA-binding protein implicated in neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer's disease (AD).
Why it matters
This review describes how loss of TDP-43's normal role in blocking cryptic exon splicing occurs before symptoms appear in diseases including ALS, FTD, and Alzheimer's disease. It presents cryptic exon inclusion as a sensitive marker of TDP-43 dysfunction that could help detect and target this problem.
-
Most common clinical diagnosis was PSP (41%) for PSP; unspecified FTD (36%) for CBD; AD for AGD (57%) and Other-4R groups (48%), without sex differences.
Why it matters
In four-repeat tauopathies, females had less cognitive decline, apathy, and motor symptoms and were older at symptom onset, while males were more likely to show Lewy body co-pathology. Both sexes had low clinical diagnostic accuracy for these tauopathies.
-
TDP-43 pathology is a hallmark of fatal neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and limbic-predominant age-related TDP-43-encephalopathy (LATE).
Why it matters
Using a cell-based reporter, this study showed that seeding-driven TDP-43 aggregation causes progressive loss of nuclear TDP-43 and features of reduced TDP-43 activity, including DNA damage and cryptic exon splicing, with similar splicing seen in human neurons. The authors describe this as a platform for finding ways to reduce TDP-43 misfolding and aggregation and limit its toxicity.
-
Mild cognitive impairment in Parkinson's disease (PD-MCI) can affect several cognitive domains, including attention, working memory, executive functions, language, visuospatial skills, and episodic memory, resulting in a progressive reduction of autonomy and an increased risk of dementia.
Why it matters
This is a design and methodology paper for the OPERA project, which will develop a robotic platform for virtual cognitive training in Parkinson's disease. No results are available yet, so it cannot yet say whether this training affects cognitive decline or dementia risk.
-
Area under the receiver operating characteristic curves differentiating PSP and controls were improved by PC1 subtraction in the frontal white matter (0.54 to 0.67; P = 0.002) and subcortical (0.69 to 0.87; P < 0.001) regions.
Why it matters
Subtracting the first principal component improved [18F]flortaucipir PET's ability to distinguish PSP from controls and increased sensitivity to 4R tau. This is a PET imaging analysis method for non-Alzheimer tauopathies, not a treatment, cure, or prevention.
-
AD patients exhibited increased expression of pyroptosis-related genes, supporting the involvement of pyroptosis in neurodegeneration.
Why it matters
In mouse models, TAU overexpression induced pyroptosis and neuroinflammation, and while GSDMD deficiency reduced pyroptosis-related markers it unexpectedly worsened synaptic plasticity deficits; DMF treatment suppressed pyroptosis gene expression, reduced GSDMD levels and alleviated neuroinflammation. The authors suggest DMF could be a therapeutic avenue in tauopathies, but this is animal and laboratory work, not a proven treatment, cure or prevention.
-
Methylglyoxal (MG), a reactive dicarbonyl metabolite associated with diabetes and metabolic disorders, contributes to carbonyl stress, neuroinflammation, and Alzheimer-like neurodegeneration.
Why it matters
In mice given methylglyoxal to mimic metabolic stress, propyl gallate improved learning and memory and reduced tau hyperphosphorylation, amyloid-beta accumulation, and inflammatory cytokines. These are animal findings, so it is not known whether this food-additive antioxidant helps people with Alzheimer's disease.
-
AD showed canonical slowing with delta/theta increases and posterior alpha loss.
Why it matters
EEG showed distinct patterns of network reorganization in Alzheimer's disease, frontotemporal dementia, and dementia with Lewy bodies, such as alpha loss in Alzheimer's and uniquely reduced gamma in dementia with Lewy bodies. The authors say these metrics may inform mechanistic models of dementia, but this is about understanding and distinguishing diseases, not treatment.
-
We show that TDP-43 activates GSK3 and promotes caspase-dependent cleavage of TDP-43, generating C-terminal fragments.
Why it matters
In laboratory neurons, blocking the enzyme GSK3 reduced harmful forms of the TDP-43 protein and improved neuron survival. This is early cell and animal work, and the authors describe GSK3 inhibition as a promising strategy that still needs testing in people.
-
In UKB, higher 2-h post-load glucose was associated with a 69% increased Alzheimer's dementia risk (odds ratio 1.69 [95% confidence interval 1.38-2.07]), though this did not replicate in an independent GWAS.
Why it matters
This study found that higher 2-hour post-load glucose was associated with increased Alzheimer's dementia risk, though this did not replicate in an independent analysis, and fasting insulin, fasting glucose, and postprandial glucose did not influence brain volumes. It suggests that postprandial hyperglycaemia may play a role in Alzheimer's risk, but it does not show that controlling glucose prevents dementia.
-
Growing evidence suggests that the APOE ε4 allele, a genetic risk factor for Alzheimer disease (AD), influences the clinical-pathologic features of Parkinson disease (PD).
Why it matters
This study looked at people newly diagnosed with Parkinson disease who carry the APOE ε4 gene variant, which is a known risk factor for Alzheimer disease. The available text does not report any treatment, cure, or prevention findings.
-
Higher total meat consumption (red meat: 51%, poultry: 20%, processed meat: 29%), was associated with a better cognitive trajectory only in the APOE34/44 stratum (β per 1 z-unit increase: 0.011; CI: 0.004 to 0.018 versus -0.003; CI: -0.008 to 0.003; P for interaction = 0.002).
Why it matters
In a Swedish longitudinal study, higher total meat consumption was associated with a better cognitive trajectory only in people with APOE ε34 or ε44 genotypes, mainly in episodic memory. This is an observational association and does not show that eating more meat prevents or treats Alzheimer's disease.
-
Due to the reduced variability in endpoints when using digital twins as covariates in statistical analyses, the TRAILBLAZER-ALZ 2 trial could have enrolled up to 24% fewer control arm participants to draw the same conclusions about treatment efficacy as previously reported for the study's primary outcome, the integrated Alzheimer Disease Rating Scale (iADRS) at 18 months.
Why it matters
This analysis of a simulated donanemab trial found that using digital twins as covariates could allow up to 24% fewer control arm participants or increase power up to 15% for secondary endpoints. These are statistical trial-design findings only and say nothing about whether any treatment cures or prevents Alzheimer's disease.
-
Whereas neurotoxic Aβ is derived from amyloid precursor protein (APP) by β- and γ-secretase cleavage, APP processing along the non-amyloidogenic pathway results in the secretion of the large neurotrophic ectodomain APPsα.
Why it matters
This study used viral and liposomal delivery of a neurotrophic peptide called CTα16 to restore spine density and synaptic plasticity in mouse models of Alzheimer's-like pathology. These are animal results, so it is too early to say whether this approach treats or prevents Alzheimer's disease in people.
-
The ALPS-index showed a stepwise decline with increasing WMH severity and cognitive impairment (p < 0.001).
Why it matters
This study found that markers of brain fluid clearance and blood vessel reactivity were worse in people with more severe white matter hyperintensities and cognitive impairment. The authors suggest that preserving vascular health and improving glymphatic clearance might help control white matter hyperintensity progression, but this is a suggestion, not a proven treatment.
-
The spreading of MAPT/Tau pathology is closely associated with the progression of neurodegeneration and cognitive decline in Alzheimer disease and other tauopathies.
Why it matters
This study established a new C. elegans model of MAPT/Tau spreading and used a genome-wide RNAi screen to identify 59 genes critical for maintaining endolysosomal integrity. The findings are from a worm model and identify genes related to the ESCRT complex, ubiquitin-proteasome system, mRNA splicing, and fatty acid metabolism.
-
42/100
We observed a nonlinear trajectory of two functional connectivity metrics-temporal variability (fluidity) and connectedness (average node strength)-across symptom severity, especially in the delta frequency band.
Why it matters
This study found that two functional connectivity measures were elevated in intermediate severity groups in early Lewy body dementia and were associated with better executive functioning, suggesting a possible compensatory role. It is about early brain changes and compensation, not about treating, curing or preventing the 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.
- Apoptosis-associated proteins p53 and APO-1/Fas (CD95) in brains of adult patients with Down syndrome
- Longitudinal fMRI in elderly reveals loss of hippocampal activation with clinical decline
- Investigating the effects of complement loci CFH and ARMS2/HTRA1 on Alzheimer Disease
- Inflammatory biomarkers are associated with total brain volume: the Framingham Heart Study
- Nasu-Hakola disease with a splicing mutation of TREM2 in a Japanese family
- P-glycoprotein deficiency at the blood-brain barrier increases amyloid-beta deposition in an Alzheimer disease mouse model
- TREM2 deficiency aggravates α-synuclein-induced neurodegeneration and neuroinflammation in Parkinson's disease models
- The Sigma-2 Receptor/TMEM97, PGRMC1, and LDL Receptor Complex Are Responsible for the Cellular Uptake of Aβ42 and Its Protein Aggregates
- RAGE (yin) versus LRP (yang) balance regulates alzheimer amyloid beta-peptide clearance through transport across the blood-brain barrier
- Gain and loss of function of ALS-related mutations of TARDBP (TDP-43) cause motor deficits in vivo