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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Graph theoretical analysis of the speech/language network showed that regions with shorter functional paths to the epicentre exhibited greater longitudinal atrophy.
Why it matters
In the non-fluent/agrammatic variant of primary progressive aphasia, regions with shorter functional paths to the epicentre showed greater longitudinal atrophy, supporting spread of neurodegeneration along network architecture. This concerns how atrophy progresses, not treating, curing, or preventing Alzheimer's disease.
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Researchers used a tau PET agent to examine tau retention patterns in cognitively normal older people and compared them with young controls and Alzheimer's disease patients.
Why it matters
Uses PET imaging to measure tau deposits in the ageing human brain. Being able to see where tau builds up in living people supports research into the disease and is not itself a treatment.
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The Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA) are the most commonly used scales to test cognitive impairment in Lewy body disease (LBD), but there is no consensus on which is best suited to assess cognition in clinical practice and most sensitive to cognitive decline.
Why it matters
This study compared the MMSE and MoCA tests for measuring thinking changes over one year in people with Lewy body disease. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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The hippocampus has been shown to demonstrate a remarkable degree of plasticity in response to a variety of tasks and experiences.
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A systematic literature review and meta-analyses (where appropriate) were performed and the GRADE approach was used to update the previous American Academy of Sleep Medicine Practice Parameters on the treatment of intrinsic circadian rhythm sleep-wake disorders.
Why it matters
This clinical practice guideline gives a second-tier positive endorsement of light therapy, with or without behavioral interventions, for elderly people with dementia, and recommends against the use of melatonin and discrete sleep-promoting medications for demented elderly patients. No recommendations were provided for remaining treatments or populations due to insufficient or absent data.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial surface receptor that triggers intracellular protein tyrosine phosphorylation.
Why it matters
A rare TREM2 gene change (R47H) is linked to a higher risk of Alzheimer's, so this study removed TREM2, fully or partly, in a mouse model of the disease (5XFAD). With less TREM2, more amyloid built up because the brain's immune cells (microglia) failed to gather around plaques and died, and the authors report that TREM2 senses lipids found with amyloid and on damaged nerve cells. This is mouse work that tested TREM2 loss rather than the R47H variant itself, and it does not test any treatment or show an effect in people.
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For neuropsychology measures, we noted the earliest significant differences between mutation carriers and non-carriers 5 years before expected onset, when differences were significant for all measures except for tests of immediate recall and verbal fluency.
Why it matters
In genetic frontotemporal dementia, the earliest significant differences between mutation carriers and non-carriers appeared about 5 years before expected onset on most neuropsychology measures. This cross-sectional study may help define markers to stage presymptomatic disease for future trials, but it reports no treatment or cure.
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Hereditary frontotemporal dementia associated with mutations in the microtubule-associated protein tau gene (MAPT) is a protean disorder.
Why it matters
This review describes how mutations in the MAPT gene cause hereditary frontotemporal dementia with three distinct neuropathologic subtypes, which is relevant for correlating imaging with tau pathology. It is a summary of disease classification and imaging, not a treatment, cure or prevention.
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62/100
Previous animal models and structural imaging investigations have linked hippocampal neuroplasticity to electroconvulsive therapy (ECT) response, but the relationship between changes in hippocampal volume and temporal coherence in the context of ECT response is unknown.
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We recommend a new term, "primary age-related tauopathy" (PART), to describe a pathology that is commonly observed in the brains of aged individuals.
Why it matters
This 2014 paper proposed the name "primary age-related tauopathy" (PART), with "working neuropathological diagnostic criteria", for brains that have Alzheimer's-type tau tangles but no amyloid plaques, and so do not meet the formal autopsy criteria for Alzheimer's disease. The authors describe it as "almost universally detectable at autopsy among elderly individuals", with symptoms that "usually range from normal to amnestic cognitive changes, with only a minority exhibiting profound impairment". At the time it "cannot be specifically identified pre-mortem", and the paper tests no treatment.
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Much of the genetic basis for Alzheimer disease (AD) is unexplained.
Why it matters
This work identified PLXNA4 as a gene associated with Alzheimer's disease and found it modulates tau phosphorylation in cell models and human brain. It points to a possible biological pathway, but it is early genetic and laboratory research, not a treatment or cure.
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Alterations in the hippocampus were evident across psychotic disorders.
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Why it matters
Reports a distinct molecular and functional signature in microglia that depends on TGF-β.
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Our results suggest that the TREM2 p.R47H substitution is a risk factor for frontotemporal dementia and Parkinson's disease in addition to Alzheimer's disease.
Why it matters
This genetic study found that the TREM2 p.R47H variant was associated with higher risk of frontotemporal dementia and Parkinson's disease, in addition to Alzheimer's disease. It identifies a shared genetic risk factor but does not provide a treatment, cure or prevention for Alzheimer's disease.
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Alzheimer's disease is the world's most common dementing illness.
Why it matters
This study reports "strongly enhanced active caspase-1" in the brains of people with mild cognitive impairment and Alzheimer's disease, which the authors say suggests a role for the inflammasome in the disease. Its title adds that NLRP3 "contributes to pathology in APP/PS1 mice", but alzhub's stored summary does not describe the mouse experiments. The human result is an association in brain tissue with no numbers given here, so it does not show that NLRP3 causes Alzheimer's or that blocking it would help patients.
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Parkinson disease (PD) is a complex neurodegenerative disorder with largely unknown genetic mechanisms.
Why it matters
This study of brain tissue from people with Parkinson disease found altered expression of the FOXO1 gene and related genes, but the samples were selected to have no significant Alzheimer disease pathology. The results are about Parkinson disease and do not provide direct evidence for Alzheimer treatment or prevention.
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Intronic expansion of the GGGGCC hexanucleotide repeat within the C9ORF72 gene causes frontotemporal dementia and amyotrophic lateral sclerosis/motor neuron disease in both familial and sporadic cases.
Why it matters
This study describes the clinical and pathological features of amyotrophic lateral sclerosis in people with C9ORF72 expansions, a genetic variant also linked to frontotemporal dementia. It does not test any treatment or prevention, and the authors note the motor neuron disease phenotype was not yet well characterized.
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Several families have been reported with autosomal-dominant frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), genetically linked to chromosome 9p21.
Why it matters
In families with inherited frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) linked to chromosome 9p21, this study found an expanded GGGGCC repeat in the C9ORF72 gene. In the authors' clinical series it was the most common genetic abnormality: 11.7% of familial FTD and 23.5% of familial ALS. The authors call it "a major cause of both FTD and ALS", though the study concerns those diseases rather than Alzheimer's and tests no treatment or prevention.
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Amyotrophic lateral sclerosis (ALS) is a paralytic and usually fatal disorder caused by motor-neuron degeneration in the brain and spinal cord.
Why it matters
Mutations in UBQLN2 were found to cause dominantly inherited, chromosome-X-linked ALS and ALS/dementia, and functional analysis showed they impair protein degradation. This links ubiquilin 2 abnormalities to abnormal protein aggregation and neurodegeneration and suggests a possible target for therapeutic intervention, but no treatment was tested.
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Amyloid-beta (Abeta) accumulation in the brain extracellular space is a hallmark of Alzheimer's disease.
Why it matters
In mice, amyloid-beta levels in brain fluid rose with wakefulness, acute sleep deprivation and orexin infusion, and fell with a drug that blocks orexin receptors. Chronic sleep restriction increased amyloid plaque formation in mice engineered to make amyloid precursor protein, and the authors suggest the sleep-wake cycle and orexin may play a role in Alzheimer's disease.
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AD patients treated with DHA-rich n-3 FAs supplementation increased their plasma concentrations of DHA (and EPA), which were associated with reduced release of IL-1beta, IL-6, and granulocyte colony-stimulating factor from PBMCs.
Why it matters
In this small substudy, six months of DHA-rich omega-3 supplementation changed blood markers of inflammation in patients with Alzheimer disease. It did not test whether this improves memory or changes the disease course.
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62/100
Multiple system tauopathy with presenile dementia (MSTD) is an inherited disease caused by a (g) to (a) transition at position +3 in intron 10 of Tau.
Why it matters
In one family carrying an inherited Tau mutation (a change at position +3 in intron 10), most of the 21 patients (17) first showed behavioural changes typical of frontotemporal dementia, memory problems were present at onset in 15, and movement problems (parkinsonism) appeared about 3 years after symptoms began. Brain scans showed the most shrinkage in memory and insular regions on the right side, and brain tissue showed deposits made mostly of "4-repeat" tau. This is a rare inherited frontotemporal dementia, not Alzheimer's disease. The study tests no treatment, and its suggestion that variation in the normal copy of the Tau gene "may" shape symptoms is unconfirmed.
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Ubiquitin-positive, tau- and alpha-synuclein-negative inclusions are hallmarks of frontotemporal lobar degeneration with ubiquitin-positive inclusions and amyotrophic lateral sclerosis.
Why it matters
Before this study, the ubiquitinated protein inside the tau- and alpha-synuclein-negative inclusions of frontotemporal lobar degeneration (FTLD-U) and ALS was unknown. The authors report that it is TDP-43, which they found in an abnormal form ("hyper-phosphorylated, ubiquitinated, and cleaved") only in affected brain and spinal cord regions. They conclude it is "the common pathologic substrate linking these neurodegenerative disorders". The study is about FTLD and ALS, not Alzheimer's disease, and it does not test any treatment, test or prevention.
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62/100
Idiopathic Parkinson's disease (PD) is a neurodegenerative disorder associated with akinesia, tremor and rigidity.
Why it matters
In 18 Parkinson's disease patients, PET imaging showed increased microglial activation in several brain regions compared with 11 controls, and this signal remained stable over 2 years in eight patients. The findings associate microglial activation with the disease process but did not test any treatment, and levels did not correlate with clinical severity.
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Unsaturated fatty acids are important constituents of neuronal cell membranes and have neuroprotective, antioxidant, and anti-inflammatory properties.
Why it matters
This study examined whether a high intake of unsaturated fatty acids is associated with a lower risk of Parkinson disease. It concerns Parkinson disease, not Alzheimer's disease, and being observational it cannot show that diet prevents 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.
- Cerebral small vessel disease genomics and its implications across the lifespan
- Hippocampal deformities in schizophrenia characterized by high dimensional brain mapping
- TREM2/DAP12 Signal Elicits Proinflammatory Response in Microglia and Exacerbates Neuropathic Pain
- Bioaccumulation of microplastics in decedent human brains
- Anti-Abeta antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic mice
- Synergistic neurotoxicity of opioids and human immunodeficiency virus-1 Tat protein in striatal neurons in vitro
- Quinolinic acid upregulates chemokine production and chemokine receptor expression in astrocytes
- Endogenous opioids in frontal cortex of patients with Down syndrome
- Temsirolimus attenuates tauopathy in vitro and in vivo by targeting tau hyperphosphorylation and autophagic clearance
- TREM2 R47H variant and risk for Alzheimer's disease: assessment in a Greek population and updated meta-analysis