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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Regional sex-related differences in tau PET burden may contribute to the disparities in AD prevalence between males and females.
Why it matters
In 148 cognitively normal older adults at one research centre, women and men had the same amount of amyloid, yet women had "significantly higher tau PET levels than males in multiple regions" — whether or not amyloid was taken into account. Women who had used hormone therapy showed "a small reduction in tau PET," but men "still had substantially lower tau PET." This is a one-time snapshot, not a trial: it suggests why Alzheimer's is more common in women but does not show that hormone therapy prevents it, and the authors call for longitudinal studies.
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It has been well established that the TMEM106B gene rs1990622 variant was a frontotemporal dementia (FTD) risk factor.
Why it matters
This work analysed genetic data to see whether the rs1990622 variant is associated with Alzheimer's disease and regulates TMEM106B expression in brain tissue. It is genetic and gene-expression analysis, so it does not test any treatment, cure or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is characterized by plaques containing amyloid-β (Aβ) and neurofibrillary tangles composed of aggregated, hyperphosphorylated tau.
Why it matters
This 2020 research paper studied how the TREM2 variant R47H affects brain inflammation ("gliosis") and nerve-cell loss driven by tau, the protein that forms tangles in Alzheimer's disease. Our stored summary covers only the background, which notes that rare TREM2 variants raise Alzheimer's risk "2- to 4-fold" and that this is "likely" because microglia respond less to amyloid. It does not include what the study found, what it was done in, or how large it was, so read the original paper before drawing any conclusion.
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Physical activity decreases the risk of a network of diseases, and exercise may be prescribed as medicine for lifestyle-related disorders such as type 2 diabetes, dementia, cardiovascular diseases, and cancer.
Why it matters
This review describes how skeletal muscle releases myokines during exercise that can affect the brain and other organs, and suggests these myokines may serve as biomarkers for monitoring exercise prescriptions. It does not test any treatment or prevention for Alzheimer's disease, so it remains early-stage knowledge about possible mechanisms.
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Exposure to ambient air pollution is a well-established determinant of health and disease.
Why it matters
This review reports growing evidence linking air pollution exposure to increased risk of stroke, dementia, Parkinson's disease, and other brain and mental health conditions. It suggests inflammation and oxidative stress may be key mechanisms, and calls for urgent measures to reduce air pollution.
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55/100
Alzheimer's disease, obesity-related metabolic syndrome, and cancer are the leading causes of death and among the most costly medical conditions in the Western world.
Why it matters
This review describes TREM2 as an immune signaling hub that senses tissue damage and highlights the potential of therapeutic manipulation of TREM2 signaling. It is a review and does not report a tested treatment, cure or prevention.
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Parkinson's disease (PD) is characterized by the accumulation of misfolded and aggregated α-synuclein (α-syn) into intraneuronal inclusions named Lewy bodies (LBs).
Why it matters
In a lab-grown neuron model built to mimic how Lewy bodies form, this study found that formation is not just α-synuclein clumping into fibrils: it also involves chemical modification of the protein and its entanglement with cell structures including mitochondria, the autophagosome and the endolysosome. The authors conclude that this whole formation process, rather than fibrils alone, "is one of the major drivers of neurodegeneration." This is a Parkinson's-framed cell study, not a human or treatment study, so it points to mechanisms worth testing rather than anything patients or families can act on directly.
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55/100
Establishing this clinical definition supports future research and investigation of an underlying mechanism.
Why it matters
This case-control study described 35 people with Down syndrome who had unexplained regression at an average age of 17.5 years, distinct from Alzheimer disease. It supports a clinical definition to guide future research and does not test treatment or cure.
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Recent advances suggest that the response of RNA metabolism to stress has an important role in the pathophysiology of neurodegenerative diseases, particularly amyotrophic lateral sclerosis, frontotemporal dementias and Alzheimer disease.
Why it matters
This review suggests that chronic stress granules, which normally are temporary, may become persistent with ageing and act as a starting point for the clumping of disease-related proteins in ALS, frontotemporal dementias, and Alzheimer's disease. It proposes a model for how problems in RNA metabolism might lead to nerve damage, but it does not test a treatment or cure.
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55/100
Obesity has been associated with increased risk of accelerated cognitive decline and dementia, which suggests underlying neurobiological changes.
Why it matters
This cross-sectional study examined associations between obesity and brain structure, including brain volumes and white matter microstructure, in a general population sample. It is observational, so it cannot show that weight loss prevents cognitive decline or dementia.
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55/100
TAR DNA-binding protein 43 (TDP-43) aggregation is the most common pathological hallmark in frontotemporal dementia (FTD) and characterizes nearly all patients with motor neuron disease (MND).
Why it matters
This study examined TDP-43 pathology in vulnerable neurons in frontotemporal dementia and suggests that loss of nuclear TDP-43 function may promote neurodegeneration. It is early-stage research in a small number of patients and does not test any treatment, cure, or prevention for Alzheimer's disease.
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SYGRAVA is the first randomized trial to determine whether programmable ASDs reduce complications of drainage compared to fixed ASDs in patients with iNPH.
Why it matters
This is a protocol comparing two valve types used in shunt surgery for idiopathic normal-pressure hydrocephalus, a different dementia from Alzheimer's. No results are available, and it does not address Alzheimer's disease treatment or prevention.
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We found increased levels of YKL-40 and decreased levels of sAPPβ in both FTD and ALS groups compared to controls.
Why it matters
In spinal-fluid samples from 86 people with frontotemporal dementia, 38 with ALS and 49 healthy controls, both patient groups had higher YKL-40 and lower sAPPβ than controls, and the sAPPβ/YKL-40 ratio tracked disease severity in FTD and brain thickness in frontotemporal regions. Neurofilament light (NfL) levels were linked to poorer thinking scores across the ALS-FTD spectrum. These are group-level associations in people whose spinal fluid did not look like Alzheimer's; the study tested no treatment and does not show these markers diagnose or predict Alzheimer's disease.
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Previous publications indicate that Alzheimer's Disease (AD) related cortical atrophy may develop in asymmetric patterns, with accentuation of the left hemisphere.
Why it matters
This longitudinal study used FDG PET to look at patterns of cerebral glucose metabolism in amyloid-positive people with mild cognitive impairment and dementia. It describes a marker of disease progression, not a treatment, cure or prevention.
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Defects in nucleocytoplasmic transport have been identified as a key pathogenic event in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) mediated by a GGGGCC hexanucleotide repeat expansion in C9ORF72, the most common genetic cause of ALS/FTD.
Why it matters
This laboratory work found that cellular stress disrupts nucleocytoplasmic transport by moving transport factors into stress granules, and that blocking stress granule assembly reduced these defects and neurodegeneration in C9ORF72-mediated ALS/FTD. It is cell and model research, so it does not yet show any treatment, cure or prevention for Alzheimer's disease.
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It is assumed that atherosclerotic arteries contain several macrophage subsets endowed with specific functions.
Why it matters
In mice bred to develop atherosclerosis (Ldlr-/-), researchers sequenced single immune cells (CD45+) from the aorta, comparing animals on a normal diet with animals after 11 weeks of a high-fat diet, and found "13 distinct aortic cell clusters". It is a map of immune cells in diseased arteries, not a brain or dementia study. It does not test any treatment, cure or prevention for Alzheimer's disease.
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However, whether large perivascular spaces (L-PVSs) (>3 mm in diameter) visible on MRI are associated with SVD and cognitive deterioration in older individuals is unknown.
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These models have revealed insights into frontotemporal dementia, Huntington's disease, multiple sclerosis, Parkinson's disease and other conditions.
Why it matters
Multimodal models have provided insights into disease progression in Alzheimer's and other neurodegenerative diseases, generally supporting the amyloid-led hypothetical model. These models are for understanding disease mechanisms and progression, not for treating, curing, or preventing Alzheimer's disease.
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TDP-43 is a primarily nuclear RNA-binding protein, whose abnormal phosphorylation and cytoplasmic aggregation characterizes affected neurons in patients with amyotrophic lateral sclerosis and frontotemporal dementia.
Why it matters
This study found that normal TDP-43 forms oligomers in the brain that prevent the formation of pathologic aggregates. It is a laboratory study and does not test any treatment or prevention for Alzheimer's disease, so it has no direct implications for treating, curing, or preventing the disease.
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55/100
Neuroinflammation is an important contributor to Alzheimer's disease (AD) pathogenesis, as underscored by the recent identification of immune-related genetic risk factors for AD, including coding variants in the gene TREM2 (triggering receptor expressed on myeloid cells 2).
Why it matters
Earlier mouse studies disagreed on whether losing the immune gene TREM2 lowers or raises amyloid. In one Alzheimer's mouse model (APPPS1-21), this 2017 study found that TREM2 deficiency "ameliorates amyloid pathology early, but exacerbates it late in disease progression". Late in the disease, fewer immune cells gathered around plaques because those cells multiplied less. This is one mouse model with no numbers or memory results in the record, and it tested no treatment in people.
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Regions with high-average SUVR are not necessarily those with the greatest tau pathology.
Why it matters
This study found that average tau PET signal varies by brain region even in younger people with little or no tau tangles, so it recommends standardizing the values. This is a technical point about interpreting tau scans, not a treatment, cure, or prevention.
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Emerging evidence supports a role for innate immunity and microglia in Alzheimer's disease (AD) pathophysiology.
Why it matters
In people with dominantly inherited Alzheimer's disease, changes in a microglia-related marker called sTREM2 in cerebrospinal fluid occurred after amyloid deposition and neuronal injury. This marker may help track the timing of the disease process, but the study did not test any treatment or cure.
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Twenty-four patients with Lewy body disease (7 DLB, 8 PD-impaired, and 9 PD-normal) underwent multimodal brain imaging, cognitive testing, and neurologic evaluation, and imaging measures were compared with those of an independently acquired group of 29 controls with minimal brain amyloid burden as measured with carbon 11-labeled Pittsburgh Compound B ([11C]PiB) positron emission tomography (PET).
Why it matters
In 24 patients with Lewy body disease, greater tau tracer uptake in certain brain regions was associated with increased cognitive impairment. This is a small cross-sectional imaging study in Lewy body diseases, not Alzheimer's disease, and it tests no treatment, cure, or prevention.
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55/100
The chronic effects of repetitive head impacts (RHI) on the development of neuroinflammation and its relationship to chronic traumatic encephalopathy (CTE) are unknown.
Why it matters
In donated brains from 66 American football players and 16 non-athlete controls, researchers counted inflammatory immune cells (microglia), astrocytes and abnormal tau in one frontal brain region to ask how repeated head impacts relate to brain inflammation, tau build-up and dementia risk in chronic traumatic encephalopathy (CTE). The authors report that microglial inflammation is linked to tau accumulation in CTE, a condition distinct from Alzheimer's disease; people with other brain diseases, including Alzheimer's, were excluded. This is an observational study of donated tissue: it shows an association, not cause and effect, and offers no treatment or prevention.
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TREM2 is a lipid-sensing activating receptor on microglia known to be important for Alzheimer's disease (AD), but whether it plays a beneficial or detrimental role in disease pathogenesis is controversial.
Why it matters
This study found that Alzheimer's-associated TREM2 variants either decreased or markedly increased binding to TREM2 ligands, while confirming increased Alzheimer's risk for several variants. It is a genetic and lab-based analysis and does not test any treatment.
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.
- Mapping limbic network organization in temporal lobe epilepsy using morphometric correlations: insights on the relation between mesiotemporal connectivity and cortical atrophy
- Soluble amyloid-beta in the brain: the scarlet pimpernel
- Cytoplasmic TDP-43 De-mixing Independent of Stress Granules Drives Inhibition of Nuclear Import, Loss of Nuclear TDP-43, and Cell Death
- Late neurological complications after prophylactic cranial irradiation in patients with small-cell lung cancer: the Toronto experience
- Functional insights from biophysical study of TREM2 interactions with apoE and Aβ1-42
- Molecular mechanisms and consequences of TDP-43 phosphorylation in neurodegeneration
- Lecanemab in symptomatic PSEN1 p.Met233Val early-onset Alzheimer's disease: Neuroimaging safety, regional amyloid-PET dynamics, and longitudinal plasma biomarkers
- Mediterranean diet and leukocyte telomere length in a multi-ethnic elderly population
- Interactions of pathological proteins in neurodegenerative diseases
- Endoplasmic reticulum stress mediates amyloid β neurotoxicity via mitochondrial cholesterol trafficking