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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For one of the primary analyses, the interpretation of the florbetapir scans (majority interpretation of five nuclear medicine physicians, who classified each scan as amyloid positive or amyloid negative) was compared with amyloid pathology (assessed according to the Consortium to Establish a Registry for Alzheimer's Disease standards, and classed as amyloid positive for moderate or frequent plaques or amyloid negative for no or sparse plaques); correlation of the image analysis results with amyloid burden was tested as a coprimary endpoint.
Why it matters
This study compared florbetapir amyloid PET scans with brain tissue examined after death, in participants "who had an autopsy within 2 years"; the measured amount of tracer correlated with the amount of amyloid found at autopsy (Spearman ρ 0.76). The authors say the results validate the yes/no visual reading of these scans approved for clinical use in the USA, which separates people with no or sparse amyloid plaques from those with moderate to frequent plaques. A negative read can therefore still mean sparse plaques, and the study was about detecting plaques, not about diagnosing dementia or treating it.
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60/100
We aimed to determine the regional pattern of brain atrophy associated with the C9ORF72 gene mutation, and to determine which regions best differentiate C9ORF72 from subjects with mutations in tau and progranulin, and from sporadic frontotemporal dementia.
Why it matters
This study found that different genetic causes of frontotemporal dementia show different patterns of brain atrophy on imaging, and suggests imaging may help tell them apart in individual patients. It concerns diagnosis and classification, not treating, curing, or preventing dementia.
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Incomplete penetrance was suggested in two kindreds, and the youngest generation had significantly earlier age of onset (>10 years) compared with the next oldest generation in 11 kindreds.
Why it matters
This study describes frontotemporal dementia and/or amyotrophic lateral sclerosis associated with the GGGGCC repeat expansion in C9ORF72, finding incomplete penetrance in two kindreds and significantly earlier age of onset in the youngest generation in 11 kindreds. Neuropathological examination of 14 patients revealed a range of TDP-43 pathology and ubiquitin-positive cerebellar granular neuron inclusions, but the study reports no treatment or cure.
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IL-6, and, to a lesser degree, CRP levels were associated with WMH severity as well as global markers of brain atrophy.
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There was, as expected, a significant association between C9ORF72 mutations and presence of motor neuron disease.
Why it matters
This study found that C9ORF72 mutations cause some but not all cases of frontotemporal dementia with motor neuron disease, and are associated with variable clinical presentations and pathology. It highlights a powerful association between C9ORF72 mutations and psychosis, suggesting the behavioural characteristics of these patients are qualitatively distinct.
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Microglia are highly motile phagocytic cells that infiltrate and take up residence in the developing brain, where they are thought to provide a surveillance and scavenging function.
Why it matters
In mice, microglia, cells that take up debris in the brain, engulfed synaptic material and played a major role in pruning synapses during development after birth. The authors suggest problems with microglia function may contribute to synapse abnormalities seen in some neurodevelopmental disorders.
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There is a clear need to develop biomarkers for Parkinson disease (PD) diagnosis, differential diagnosis of Parkinsonian disorders, and monitoring disease progression.
Why it matters
This cross-sectional study measured total tau, phosphorylated tau, amyloid beta peptide 1-42, Flt3 ligand and fractalkine levels in cerebrospinal fluid in Parkinson disease patients and controls. It is about Parkinson disease diagnosis and progression, so it does not provide evidence about treating, curing or preventing Alzheimer's disease.
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The findings indicate for the first time in humans that PTSD is associated with selective volume loss of the CA3/dentate gyrus subfields, consistent with animal studies, implying that chronic stress suppresses neurogenesis and dendritic branching in these structures.
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This preliminary report suggests that CETP V405 valine homozygosity is associated with slower memory decline and lower incident dementia and AD risk.
Why it matters
In this cohort of older adults without dementia, a variant in the CETP gene was tested for links to memory decline and dementia risk. The study is observational, so it cannot show that changing this gene or related cholesterol pathways would prevent Alzheimer disease.
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Mutations in the progranulin gene (GRN) are an important cause of frontotemporal lobar degeneration (FTLD) with ubiquitin and TAR DNA-binding protein 43 (TDP43)-positive pathology.
Why it matters
Low levels of progranulin in plasma were found in people with progranulin mutations, including some without symptoms, and one person with probable Alzheimer's disease was identified. This is a biomarker finding only and does not show any treatment, cure or prevention for Alzheimer's disease.
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Despite its being one of the most commonly observed neurological disorders, neuropathological studies of essential tremor (ET) are rare.
Why it matters
In this comparison of 33 essential tremor brains and 21 control brains, most essential tremor cases without Lewy bodies had loss of Purkinje cells and more Purkinje cell torpedoes than controls. The study concerns essential tremor, not Alzheimer's disease, and reports no treatment or cure.
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We hypothesized that telomere length might thus relate to increased risk for dementia and mortality.
Why it matters
In this nested case-control study, shorter leukocyte telomere length was associated with both dementia and mortality. The authors suggest telomere length may be a marker of biological aging, but this does not establish a treatment, cure or prevention.
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Interferon-gamma-inducible protein 10 is specifically increased in MCI and seems to decrease with the progression of AD, whereas MCP-1 and IL-8 are up-regulated also in late stages of the disease, suggesting a role in phases in which neurodegeneration is prevalent.
Why it matters
In people with amnestic mild cognitive impairment and mild Alzheimer's disease, levels of a chemokine called IP-10 were increased in the cerebrospinal fluid, suggesting inflammation occurs early. This finding does not show that treating inflammation prevents or cures the disease.
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Hyperhomocysteinemia is associated with an increased risk of vascular disease, and recent results suggest that it also could increase the risk of dementia.
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This study examined how natural oligomers of human amyloid beta protein are formed, secreted, and affect synaptic function.
Why it matters
Reports that naturally secreted oligomers (small clumps) of amyloid beta protein strongly inhibited long-term potentiation in the hippocampus in vivo.
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A significant portion of sleep-disordered breathing is associated with ApoE epsilon4 in the general population.
Why it matters
In a general population sample of middle-aged adults, carrying the APOE epsilon4 allele was linked to a higher chance of moderate-to-severe sleep-disordered breathing. This describes an association between a risk gene and sleep problems and does not provide a treatment or prevention for Alzheimer's disease.
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60/100
Why it matters
Reports that alpha-synuclein is found in Lewy bodies.
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Plasma p-tau217 concentrations, considered together with APOE genotype, might help stratify risk and estimate the timing of future cognitive impairment in asymptomatic individuals who are at increased risk for Alzheimer's disease, such as those with a family history of dementia or known APOE-ε4 carrier status.
Why it matters
Across seven multi-ethnic cohorts, higher blood p-tau217 levels were linked to cognitive impairment and to a shorter time until impairment, with stronger links in people carrying the APOE-ε4 gene. The authors suggest p-tau217 together with APOE genotype might help estimate risk and timing of future cognitive impairment.
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These results suggest that all adults with Down syndrome should be screened for Alzheimer's disease pathology starting shortly before age 40 years and considered for clinical trials.
Why it matters
These results suggest that all adults with Down syndrome should be screened for Alzheimer's disease pathology starting shortly before age 40 and considered for clinical trials. No treatment or prevention is tested in this work.
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Accurate diagnosis of dementia with Lewy bodies (DLB) remains challenging, with misdiagnosis potentially leading to harmful treatment decisions.
Why it matters
This study developed and validated two immunoassays showing that cerebrospinal fluid DOPA decarboxylase levels are higher in dementia with Lewy bodies and Parkinson's disease than in controls or Alzheimer's disease. This is a diagnostic biomarker for Lewy body disorders and does not address treating, curing or preventing Alzheimer's disease.
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Neuro-inflammation was not reduced between the neflamapimod and placebo groups, and no change was observed in [18F]-DPA-714 PET.
Why it matters
In this exploratory trial in early Alzheimer's, the anti-inflammatory drug neflamapimod (40 mg twice-daily) did not reduce brain inflammation on PET scans and instead raised spinal fluid GFAP, a marker of reactive astrocytes (support cells). Three cases of spinal fluid inflammation (pleocytosis) occurred on the drug. The authors suggest it interfered with immune defence, which may help explain why earlier anti-inflammatory approaches failed, and urge inflammation biomarkers in future trials.
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Plasma GFAP and pTau biomarkers (pTau181, pTau231, pTau217) are significantly elevated in Aβ-positive individuals, with stronger Aβ–pTau associations observed in APOE ε4 carriers (CPAS: β = 0.26, p = 0.003 for pTau231; ADNI: β = 0.45, p < 0.001 for pTau181).
Why it matters
Across two cohorts, plasma GFAP strengthened the associations between pTau biomarkers and Tau PET, with this modulatory effect more pronounced in APOE ε4 non-carriers, and longitudinal analyses showed stronger pTau181-associated tau accumulation in people with high GFAP. The work supports the use of plasma biomarkers for diagnosis and prognosis and highlights reactive astrogliosis in tau propagation, but does not test a treatment.
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α-Synuclein seed amplification assays (αSAAs) can improve the diagnosis of synucleinopathies and detect α-synuclein (αSyn) copathology in vivo in clinical practice.
Why it matters
This study assessed how well a spinal fluid test detects alpha-synuclein in people with cognitive impairment, including those who also have Alzheimer's pathology. It is a diagnostic study and does not provide a treatment or cure.
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In SURMOUNT-5, treatment with tirzepatide was associated with greater predicted 10-year CVD risk reduction compared with semaglutide.
Why it matters
This post-hoc analysis of the SURMOUNT-5 trial is about obesity and predicted cardiovascular risk, not Alzheimer's disease. It found tirzepatide was associated with a greater reduction in predicted 10-year cardiovascular disease risk than semaglutide.
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Microglia are the resident immune cells in the brain and have pivotal roles in neurodevelopment and neuroinflammation 1,2 .
Why it matters
In mouse models, deleting Havcr2 in microglia increased phagocytic activity and ameliorated cognitive impairment and reduced amyloid-beta pathology in 5xFAD mice. These findings in a transgenic animal model highlight the therapeutic potential of targeting microglial TIM-3, but no human treatment or prevention is demonstrated.
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.
- Expansion of intronic GGCCTG hexanucleotide repeat in NOP56 causes SCA36, a type of spinocerebellar ataxia accompanied by motor neuron involvement
- Gene-expression profile of the ageing brain in mice
- Retinal microvascular signs and 10-year risk of cerebral atrophy: the Atherosclerosis Risk in Communities (ARIC) study
- HẠT NANO VÀNG VỎ ĐỒNG VÀ SINH PHẨM TÁI TỔ HỢP: TRIỂN VỌNG CHO XÉT NGHIỆM NHANH ĐỘ NHẠY CAO
- Coding variants in TREM2 increase risk for Alzheimer's disease
- Lecanemab (BAN2401): an anti-beta-amyloid monoclonal antibody for the treatment of Alzheimer disease
- Higher neighborhood deprivation is associated with accelerated disease progression in behavioral-variant frontotemporal degeneration
- Regulatory role of the endocannabinoid system on glial cells toward cognitive function in Alzheimer's disease: A systematic review and meta-analysis of animal studies
- Perinatal iron deficiency results in altered developmental expression of genes mediating energy metabolism and neuronal morphogenesis in hippocampus