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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A thinner RNFL was associated with worse cognitive performance on baseline assessment.
Why it matters
This study found that a thinner retinal nerve fiber layer was associated with worse cognitive performance at baseline and greater likelihood of future cognitive decline in people without neurodegenerative disease. It identifies a possible marker but does not test any treatment or prevention.
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Environmental enrichment may slow cognitive decay possibly acting through an improvement in vascular function.
Why it matters
A 7-month cognitive, social, and physical training programme improved cognitive scores and vascular function in people with mild cognitive impairment, especially those with hypertension. This is a multidomain lifestyle intervention for symptom improvement, not a cure or prevention.
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Reversible phase separation underpins the role of FUS in ribonucleoprotein granules and other membrane-free organelles and is, in part, driven by the intrinsically disordered low-complexity (LC) domain of FUS.
Why it matters
In this laboratory work, a protein called FUS can clump into stable gels when a chemical mark called methylation is lost, and this disrupts nerve cell function and protein production. A chaperone protein called transportin can reduce this clumping, suggesting a possible target, but this is early mechanistic research, not a treatment tested in patients.
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Tau PET shows higher magnitude of binding in MAPT mutation carriers who harbor mutations that are more likely to produce AD-like tau pathology (e.g., in our series, the non-exon 10 families tend to accumulate mixed 3R/4R aggregates).
Why it matters
This small case-control study found that tau PET signal differed among people with Alzheimer's disease, clinically normal participants, and MAPT mutation carriers, with higher binding in carriers whose mutations tend to produce AD-like tau pathology. It is about imaging tau in rare genetic forms of disease, not about treating, curing, or preventing Alzheimer's disease.
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Memory loss is one of the first symptoms of typical Alzheimer's disease (AD), for which there are no effective therapies available.
Why it matters
In this small two-week trial of 14 patients with early Alzheimer disease, repetitive transcranial magnetic stimulation of the precuneus produced a selective improvement in episodic memory but not other cognitive domains. The findings are preliminary and come from a very small sample.
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Elevated risk of developing Alzheimer's disease (AD) is associated with hypomorphic variants of TREM2, a surface receptor required for microglial responses to neurodegeneration, including proliferation, survival, clustering, and phagocytosis.
Why it matters
Weakened versions of the TREM2 gene raise Alzheimer's risk, and this study found that brain immune cells (microglia) from patients carrying these variants, and from TREM2-lacking mice with Alzheimer's-like changes, were packed with autophagic vesicles, a sign of the cell's self-digestion system running abnormally. Lab analyses linked this to faulty mTOR signalling, which affects the cells' energy (ATP) and building-block supply. Activating a different receptor (Dectin-1) or adding cyclocreatine, a creatine-like compound, offset the problem only in cells grown in a dish, so this explains a possible mechanism and does not show any treatment works in people.
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Amyotrophic lateral sclerosis is characterised by the progressive loss of motor neurons in the brain and spinal cord.
Why it matters
This review describes amyotrophic lateral sclerosis as a progressive loss of motor neurons that shares features with frontotemporal dementia and involves many different genes and processes. It states that understanding this heterogeneity is necessary to find effective treatments, but reports no treatment, cure or prevention.
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Researchers conducted a trial to test the effect of omega 3 polyunsaturated fatty acid supplementation and a multidomain intervention, alone or in combination, compared with placebo, on cognitive decline in elderly adults with memory complaints.
Why it matters
A randomised, placebo-controlled trial (MAPT) testing long-term omega 3 fatty acid supplements, with or without a multidomain intervention, on thinking skills in older adults with memory complaints.
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The aim of this study was to assess the agreement between data on cerebral amyloidosis, derived using Pittsburgh compound B positron emission tomography and (i) multi-laboratory INNOTEST enzyme linked immunosorbent assay derived cerebrospinal fluid concentrations of amyloid-β42; (ii) centrally measured cerebrospinal fluid amyloid-β42 using a Meso Scale Discovery enzyme linked immunosorbent assay; and (iii) cerebrospinal fluid amyloid-β42 centrally measured using an antibody-independent mass spectrometry-based reference method.
Why it matters
This multicentre study compared amyloid measured by Pittsburgh compound B PET imaging with several cerebrospinal fluid amyloid-β42 methods in people with normal cognition, mild cognitive impairment and various dementias. Agreement was high in mild cognitive impairment and Alzheimer's disease but more variable in cognitively normal and non-Alzheimer's groups, so these amyloid biomarkers may not always agree.
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Tauopathies, including frontotemporal dementia (FTD) and Alzheimer's disease (AD), are neurodegenerative diseases in which tau fibrils accumulate.
Why it matters
In a mouse model of frontotemporal dementia, giving salsalate after disease onset lowered total tau and tau acetylated at K174, rescued memory deficits and prevented hippocampal atrophy, and these effects were diminished in neurons expressing K174Q tau. This identifies tau acetylation as a possible therapeutic target, but the work was done in mice and is not yet a proven treatment for people.
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C9orf72 mutations are the most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
Why it matters
C9orf72 mutations are the most common cause of ALS and frontotemporal dementia, and the abnormal "dipeptide repeat" proteins they produce damage nerve cells in lab and animal models. Two unbiased screens in yeast found genes that strongly change how toxic these proteins are, including karyopherins and other parts of the Ran-mediated system that moves molecules into and out of the cell nucleus. This is early, yeast-only work that points to possible disease mechanisms and drug targets for ALS/FTD. It is not a treatment, and it does not study Alzheimer's.
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Alzheimer disease (AD) is characterized by the accumulation of amyloid plaques, which are predominantly composed of amyloid-β peptide.
Why it matters
This study describes a new physiological APP processing pathway that generates fragments capable of inhibiting neuronal activity in the hippocampus. It identifies a basic biological process but does not test or suggest any treatment, cure, or prevention for Alzheimer's disease.
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Longitudinal analysis revealed progressive and widespread changes in the grey matter, notably including the basal ganglia.
Why it matters
Longitudinal MRI in amyotrophic lateral sclerosis showed progressive and widespread grey matter changes, including the basal ganglia, across apparently sporadic patients rather than being genotype-specific. This concerns amyotrophic lateral sclerosis and has implications for MRI biomarkers, not for treating, curing, or preventing Alzheimer's disease.
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Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used agents in clinical practice.
Why it matters
This paper reviews the neurological effects associated with nonsteroidal anti-inflammatory drug use, including acute central nervous system toxicity. It does not report any treatment, cure, or prevention for Alzheimer's disease.
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This study used direct RNA sequencing without amplification or cDNA synthesis to analyze the quantitative transcriptomes of microglia in healthy adult and aged mice.
Why it matters
In mice, this study mapped the set of microglial genes it calls the sensome, which lets these immune cells of the brain sense their surroundings, and found that it shifts with age. It is basic mouse research that helps explain how brain immune cells change with aging; it does not test a treatment for Alzheimer's.
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Our results indicate that even in the absence of manifest type 2 diabetes mellitus or impaired glucose tolerance, chronically higher blood glucose levels exert a negative influence on cognition, possibly mediated by structural changes in learning-relevant brain areas.
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The hippocampus is critically involved in episodic memory, yet relatively little is known about how the development of this structure contributes to the development of episodic memory during middle to late childhood.
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The pathway leading from soluble and monomeric to hyperphosphorylated, insoluble and filamentous tau protein is at the centre of many human neurodegenerative diseases, collectively referred to as tauopathies.
Why it matters
This review states that inherited MAPT mutations cause forms of frontotemporal dementia and parkinsonism, showing tau dysfunction is sufficient to cause neurodegeneration, and that tau aggregates may spread in a prion-like manner. It notes that preventing tau aggregation and propagation is the focus of attempts to develop mechanism-based treatments, but reports no treatment, cure or prevention.
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The term cerebral small vessel disease (SVD) describes a range of neuroimaging, pathological, and associated clinical features.
Why it matters
This review discusses what brain imaging reveals about small vessel disease, which can cause dementia, but notes that the underlying mechanisms are largely unknown. It proposes ideas for future study rather than testing any treatment or prevention.
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Our findings indicate that in most patients diagnosed with IRBD this parasomnia represents the prodromal phase of a Lewy body disorder.
Why it matters
This observational cohort study found that in most patients diagnosed with idiopathic REM sleep behaviour disorder, the condition represents the prodromal phase of a Lewy body disorder. It is about identifying an early phase of disease, not about treating, curing, or preventing Alzheimer's disease.
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59/100
Expansion of a GGGGCC hexanucleotide repeat upstream of the C9orf72 coding region is the most common cause of familial frontotemporal lobar degeneration and amyotrophic lateral sclerosis (FTLD/ALS), but the pathomechanisms involved are unknown.
Why it matters
In people with the C9orf72 repeat expansion, the most common inherited cause of frontotemporal lobar degeneration and ALS, the proteins at the core of most brain inclusions were unknown. This study found that most of these inclusions contain abnormal dipeptide-repeat proteins, mainly poly-(Gly-Ala), with less poly-(Gly-Pro) and poly-(Gly-Arg), which the authors say are "presumably" made directly from the expanded repeat. This links the mutation to the main pathology in these patients, but it does not show that the proteins cause the disease, and it is not a study of Alzheimer's disease.
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This study investigated the role of microglia in remodeling synapses within the developing brain.
Why it matters
Reports that microglia shape neural circuits after birth in a way that depends on neural activity and the complement system.
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Why it matters
Proposes a harmonized classification system for FTLD-TDP pathology.
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59/100
In addition to known candidate genes, APOE, TOMM40, and one hypothetical gene LOC100129500 partially overlapping APOE; one novel gene, EPC2, and several other interesting genes were associated with CSF biomarkers that are related to AD.
Why it matters
This genome-wide study found that variations in the APOE, TOMM40, LOC100129500 and EPC2 gene regions were linked to spinal fluid markers of Alzheimer's disease. These findings concern the genetics behind these markers and do not provide a treatment, cure or prevention.
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In this large cohort study of elderly subjects, the degree of dVRS appears independently associated with age, hypertension, volume of white matter hyperintensities, and lacunar infarctions. dVRS should be considered as another MRI marker of cerebral small vessel disease in the elderly with regional variations in their severity.
Why it matters
In this population-based study of stroke- and dementia-free elderly people, more severe dilated Virchow-Robin spaces were associated with older age, higher blood pressure, and other MRI markers of small vessel disease. It identifies associations with brain small vessel disease markers, not a treatment, cure, or prevention for Alzheimer's 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.
- Electrical stimulation of the vagus nerve improves amyloid pathology in delirium superimposed on dementia
- Synaptophysin and synaptojanin-1 in Down syndrome are differentially affected by Alzheimer's disease
- APOE4 exacerbates synapse loss and neurodegeneration in Alzheimer's disease patient iPSC-derived cerebral organoids
- Rivastigmine for gait stability in patients with Parkinson's disease (ReSPonD): a randomised, double-blind, placebo-controlled, phase 2 trial
- Pomegranate polyphenols and extract inhibit nuclear factor of activated T-cell activity and microglial activation in vitro and in a transgenic mouse model of Alzheimer disease
- Oxidative Stress and Down Syndrome: A Route toward Alzheimer-Like Dementia
- U-box protein carboxyl terminus of Hsc70-interacting protein (CHIP) mediates poly-ubiquitylation preferentially on four-repeat Tau and is involved in neurodegeneration of tauopathy
- Association of total tau and phosphorylated tau 181 protein levels in cerebrospinal fluid with cerebral atrophy in mild cognitive impairment and Alzheimer disease
- Structural Plasticity of the Hippocampus and Amygdala Induced by Electroconvulsive Therapy in Major Depression
- TREM2: A new player in the tumor microenvironment