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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An optimized immunoassay was used to analyze CSF Ng in a retrospective cohort of 331 participants with different neurodegenerative diseases, including healthy controls (n = 19), biomarker-proven Alzheimer disease (AD) (n = 100), genetic AD (n = 2), behavioral variant frontotemporal dementia (n = 20), speech variant frontotemporal dementia (n = 21), Lewy body dementia (n = 13), Parkinson disease (n = 31), progressive supranuclear palsy (n = 46), multiple system atrophy (n = 29), as well as a heterogeneous group with non-neurodegenerative cognitive impairment (n = 50).
Why it matters
This study found that higher cerebrospinal fluid neurogranin concentration was specific to Alzheimer's disease and not seen in other neurodegenerative diseases. It is about a potential diagnostic marker, not about treating, curing or preventing the disease.
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Recently, several large randomised controlled trials about the treatments of cognitive impairment or dementia due to Parkinson's disease (CIND-PD or PDD) and dementia with Lewy bodies (DLB) were completed.
Why it matters
This systematic review and meta-analysis examined trials of cholinesterase inhibitors and memantine for cognitive impairment in Parkinson's disease and dementia with Lewy bodies. It assesses existing drugs for these related conditions, not for curing or preventing Alzheimer's disease.
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Circulating homocysteine levels (tHcy), a product of the folate one carbon metabolism pathway (FOCM) through the demethylation of methionine, are heritable and are associated with an increased risk of common diseases such as stroke, cardiovascular disease (CVD), cancer and dementia.
Why it matters
This study identified genetic factors related to homocysteine and methionine metabolism and a new association with ischemic stroke. It does not show that lowering homocysteine prevents dementia, and dementia is mentioned only as a disease associated with higher homocysteine levels.
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66/100
A higher omega-3 index was correlated with larger total normal brain volume and hippocampal volume in postmenopausal women measured 8 years later.
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Neurodegeneration rather than cerebrovascular lesions may play a key role in T2DM-related cognitive impairment.
Why it matters
In this cross-sectional study, type 2 diabetes was associated with more cerebral infarcts and lower total gray, white, and hippocampal volumes, with cortical atrophy resembling patterns seen in preclinical Alzheimer disease. The findings suggest neurodegeneration rather than cerebrovascular lesions may play a key role in diabetes-related cognitive impairment.
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Depressive symptoms may increase the risk of progressing from mild cognitive impairment (MCI) to dementia.
Why it matters
In this 6-month trial of 50 people with mild cognitive impairment, depressive symptoms improved in the EPA and DHA groups and verbal fluency improved in the DHA group compared with the linoleic acid group. There were no treatment effects on other cognitive or quality-of-life measures.
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66/100
Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia.
Why it matters
In a genome-wide association study of 515 people with frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP), common DNA variants in a region of chromosome 7p21 containing the gene TMEM106B were linked to the disease (top variant rs1990622, P = 1.08 × 10⁻¹¹), and the link was repeated in a further 89 cases. The authors say their data "implicate variants in TMEM106B as a strong risk factor for FTLD-TDP", and propose that the variants "may" act by increasing TMEM106B expression. This is an inherited genetic association in frontotemporal dementia, not Alzheimer's disease. It does not identify anything a person can change, and it tests no treatment, test or prevention.
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This double-blind randomized controlled trial of vitamin therapy demonstrates a strong correlation between serum tHcy and plasma Abeta40 concentrations in subjects with ischemic stroke.
Why it matters
This study found that vitamin supplementation lowered homocysteine levels but did not change plasma amyloid-beta levels, and amyloid measures were not associated with cognitive change. It does not support vitamin supplementation as a way to modify Alzheimer-related proteins or cognition.
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Evidence suggests that a high concentration of C-reactive protein (CRP) is a cardiovascular risk factor and an important correlate of cognitive disorders and depression.
Why it matters
This systematic review found that high C-reactive protein concentrations were associated with increased risk of stroke and cognitive impairment, and were predictive of cognitive decline and dementia. These are observational associations, not evidence that lowering CRP treats, cures, or prevents Alzheimer's disease.
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This longitudinal quantitative magnetic resonance imaging study of 24 patients with mild temporal lobe epilepsy shows an ipsilateral hippocampal volume decrease of 9% (range, -30 to +0.5%; p = 0.002, paired t test) over a period of 3.5 +/- 0.7 years.
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In the UGOT cohort, the optimal cutoff improved diagnostic accuracy compared with the standard single cutoff, particularly in CKD and anemia (CKD: from 0.65; 95% CI, 0.57-0.72; to 0.83; 95% CI, 0.76-0.89; anemia: from 0.80; 95% CI, 0.76-0.84; to 0.86; 95% CI, 0.82-0.90), with consistent findings in the Roche cohort.
Why it matters
This study found that using two cutoff values instead of one for the blood marker p-tau217 improved diagnostic accuracy, especially in people with chronic kidney disease or anemia. The double-cutoff approach reduced false classifications but produced intermediate results in 12% to 39% of cases.
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Greater neighborhood disadvantage was associated with elevated inflammatory and AD CSF biomarkers cross-sectionally and longitudinal increases in a nonspecific inflammatory blood biomarker.
Why it matters
In 334 older adults, greater neighborhood disadvantage was linked to higher CSF markers of inflammation and tau. This is an observational study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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65/100
Based on positive/negative results on the different biomarkers, subjects were classified as 'AD-LB-' (n = 304), 'AD+LB-' (n = 335), 'AD+LB+' (n = 158) and 'AD-LB+' (n = 68).
Why it matters
Lewy body co-pathology in Alzheimer's disease was associated with more severe hypometabolism and faster cognitive decline, but did not affect the regional hypometabolic pattern or cognitive profile. These findings indicate the presence of Lewy body pathology may have different consequences depending on Alzheimer's disease co-morbidity, with implications for accurate diagnosis.
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Previous studies have suggested that systemic viral infections may increase risks of dementia.
Why it matters
This case-control study measured plasma biomarkers linked to Alzheimer's disease pathology in UK Biobank participants before and after serology-confirmed SARS-CoV-2 infection, finding changes associated with beta-amyloid pathology. It is an observational biomarker study, so it cannot show that preventing infection prevents dementia.
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65/100
Previous studies have shown that limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) increases with age, but there have been only a few studies, which have investigated this entity in a population-based setting.
Why it matters
In this population-based study, limbic-predominant age-related TDP-43 encephalopathy neuropathologic change stages were significantly associated with dementia and lower MMSE scores, and its attributable risk was higher than that of Alzheimer's disease neuropathologic change (24.2% versus 18.6%). The study shows this pathology is very common and a major determinant of dementia in the general late-life population, but it examines brain tissue after death and tests no treatment.
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Blood-based biomarkers for Alzheimer's disease (AD) pathology have been investigated intensively as markers for AD-related neurodegeneration.
Why it matters
In people with idiopathic REM sleep behaviour disorder, lower baseline plasma Aβ42/40 ratio and higher pTau181 levels were found in those who later developed a neurodegenerative syndrome including dementia with Lewy bodies. This suggests blood markers may help predict conversion, but the study was a single-centre cohort and did not test any treatment.
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The objective is to identify risk factors associated with PASC/long-COVID diagnosis.
Why it matters
This study identified risk factors associated with post-acute sequelae of SARS-CoV-2, finding that dementia was among the characteristics associated with a lower likelihood of PASC diagnosis or care at a long-COVID clinic. It concerns long-COVID risk factors, not the treatment, cure, or prevention of Alzheimer's disease.
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Choroid plexus (ChP) is emerging as a key brain structure in the pathophysiology of neurodegenerative disorders.
Why it matters
This observational study looked at the size of the choroid plexus in the brain in patients with frontotemporal lobar degeneration and its link to other biomarkers. It is about a different dementia (FTLD), not Alzheimer's, and does not test any treatment, cure, or prevention.
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In this largely presymptomatic population, these results suggest subtle differences across plasma p-tau species and platforms for the prediction of amyloid and tau PET and magnetic resonance imaging measures of cerebrovascular and Alzheimer-related pathology.
Why it matters
In a largely presymptomatic population, plasma p-tau species and platforms showed subtle differences for predicting amyloid and tau PET and MRI measures of cerebrovascular and Alzheimer-related pathology. This is about biomarker comparison for prediction, not treatment, cure or prevention.
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Plasma p-tau217 and p-tau181 were correlated (r=0·90, p diff =0·31) and in pathology-confirmed Alzheimer's disease (n=15, mean age 73 years [SD 12]) versus pathologically confirmed FTLD (n=68, mean age 67 years [SD 8]; AUC=0·96 [0·92-1·00] for p-tau217, AUC=0·91 [0·82-1·00] for p-tau181; p diff =0·22).
Why it matters
This study found that plasma p-tau217 and p-tau181 both distinguished Alzheimer's disease from frontotemporal lobar degeneration well, with some evidence favouring p-tau217. It concerns blood biomarkers for diagnosis and does not test any treatment, cure or prevention for Alzheimer's disease.
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In this longitudinal study, we included 396 cognitively normal to dementia subjects with 18 F-Florbetapir/ 18 F-Florbetaben-amyloid-PET, 18 F-Flortaucipir-tau-PET and ~ 2-year cognitive follow-up.
Why it matters
Tau-PET and Braak-staging were highly predictive of future cognitive decline in this group of 396 people followed for about 2 years. The authors describe tau-PET as a promising marker, but this is a prognostic tool for predicting decline, not a treatment or cure.
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We found that severe COVID-19 infection, associated with a high mortality rate, might develop in a minority of fully vaccinated individuals with multiple co-morbidities.
Why it matters
This study describes 152 fully vaccinated patients hospitalized with COVID-19 in Israel, noting that 19% had dementia among their co-morbidities. It concerns COVID-19 outcomes in vaccinated people and provides no information on treating, curing, or preventing Alzheimer's disease.
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The category of neocortical LP according to the LPC system was associated with a 5.9 OR (p < 0.0001) of dementia in the 134 NBTR cases and a 3.14 OR (p = 0.0001) in the 202 UPBB cases.
Why it matters
This multi-centre study found that the neocortical Lewy pathology category was associated with higher odds of dementia in two case sets. The authors suggest this system should be the standard future approach for basic post-mortem evaluation of Lewy pathology, so it concerns diagnosis after death rather than treatment, cure or prevention.
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The insular cortex is proposed to function as a central brain hub characterized by wide-spread connections and diverse functional roles.
Why it matters
This systematic review and meta-analysis examined insular cortex atrophy patterns across frontotemporal dementia, Alzheimer's disease, Parkinson's disease and dementia with Lewy bodies, and contrast analyses did not reveal significant differences between disease groups. It describes brain changes associated with these diseases and does not test any treatment, cure or prevention.
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65/100
Plasma NfL is superior to plasma t-tau for the diagnosis and prediction of clinical progression of FTLD-S and AD-S. Classification of evidence This study provides Class III evidence that plasma NfL has superior diagnostic and prognostic performance vs plasma t-tau in FTLD and AD.
Why it matters
In 265 participants, plasma NfL but not plasma t-tau discriminated frontotemporal lobar degeneration and Alzheimer disease from healthy controls, and both were poor at telling the two apart. Plasma NfL predicted clinical decline and survival, but this concerns diagnosis and prognosis, not treatment, cure or prevention.
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.
- The endogenous tryptophan metabolite and NAD+ precursor quinolinic acid confers resistance of gliomas to oxidative stress
- Genome-Wide Association Studies of ARIA From the Aducanumab Phase 3 ENGAGE and EMERGE Studies
- Astrocytosis precedes amyloid plaque deposition in Alzheimer APPswe transgenic mouse brain: a correlative positron emission tomography and in vitro imaging study
- Soluble TREM2 in CSF and its association with other biomarkers and cognition in autosomal-dominant Alzheimer's disease: a longitudinal observational study
- Neurophysiological markers of cholinergic dysfunction in pre‐symptomatic autosomal dominant Alzheimer´s disease using Transcranial Magnetic Stimulation (TMS): research design and preliminary results
- Neurological Disease as a Failure of Brain-Immune Crosstalk: The Multiple Faces of Neuroinflammation
- Neuroinflammation: the role and consequences
- Imaging Abeta plaques in living transgenic mice with multiphoton microscopy and methoxy-X04, a systemically administered Congo red derivative
- Neural stem cells genetically-modified to express neprilysin reduce pathology in Alzheimer transgenic models
- Preclinical Catecholaminergic Biomarkers of Central Lewy Body Diseases