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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51/100
The benefits of regular exercise, physical fitness and sports participation on cardiovascular and brain health are undeniable.
Why it matters
This review states that regular exercise and sports participation improve cognition and reduce the risk of developing dementia, but also notes that repetitive mild traumatic brain injuries from sports can occasionally lead to chronic traumatic encephalopathy. It presents both the cognitive benefits and the neurological risks of sports participation rather than a treatment for dementia.
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Alzheimer's disease (AD) is the most prevalent form of dementia in the elderly population.
Why it matters
This paper discusses evidence that impaired clearance of amyloid-β, rather than its production, is responsible for late-onset Alzheimer's disease, and examines the role of the endocytic receptor LRP1 in neuronal clearance. It is a review of clearance mechanisms and does not report any treatment, cure or prevention.
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We and other members of the Alzheimer’s Disease Genetics Consortium assembled multiple data sets from a total of 5896 black patients (1968 cases and 3928 controls).
Why it matters
Describes how members of the Alzheimer's Disease Genetics Consortium tested variants in the TREM2 gene for association with Alzheimer's disease in data sets from 5896 black participants (1968 cases and 3928 controls).
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Recent studies have reported that a rare mutation of triggering receptor expressed on myeloid cells 2 gene (TREM2 [rs75932628-T]) has significantly increased the risk of late-onset Alzhemier's disease (LOAD) in European-descendent population.
Why it matters
The TREM2 R47H variant (rs75932628-T), linked to higher late-onset Alzheimer's risk in people of European descent, was absent from this study of 1,133 patients and 1,159 controls of northern Han Chinese descent. Sequencing exon 2 of TREM2 turned up four previously unreported variants, but none was significantly associated with Alzheimer's risk after Bonferroni correction. This suggests the European R47H finding may not carry over to this population; it does not rule out other TREM2 variants or show any treatment.
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Both Aβ and tau pathology affect default mode network integrity before clinical onset of Alzheimer disease.
Why it matters
In 207 cognitively normal older adults, lower spinal fluid amyloid and higher phosphorylated tau were each linked to reduced default mode network connectivity on brain scans. This is a cross-sectional association study and does not show that these brain changes cause dementia or that any treatment can reverse them.
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Rare variants in TREM2 cause susceptibility to late-onset Alzheimer's disease.
Why it matters
Using brain expression data from 101 neuropathologically normal individuals, this study found a preserved TREM2-containing module related to microglia, with TREM2 acting as a hub gene in five brain regions including the hippocampus. It describes TREM2 biology in normal human brain and reports no treatment, cure or prevention.
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TDP-43 is the major component protein of ubiquitin-positive inclusions in brains of patients with frontotemporal lobar degeneration (FTLD-TDP) or amyotrophic lateral sclerosis (ALS).
Why it matters
TDP-43 clumps taken from the brains of people with ALS or frontotemporal lobar degeneration (FTLD-TDP) made TDP-43 clump in cultured cells "in a self-templating manner", and the clumps formed in those cells could seed the process again. The seeding fragments were "characteristic of each disease type", and one subtype survived boiling. The authors conclude TDP-43 has prion-like properties that "may play a role" in disease progression. This was a cell-culture study of ALS/FTLD brain material, not of Alzheimer's, and it tested no treatment.
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Emotional changes are common in mild cognitive impairment (MCI) and Alzheimer's disease (AD).
Why it matters
In 237 participants, emotional contagion was higher at each stage from healthy controls to mild cognitive impairment to Alzheimer's disease, and higher emotional contagion was associated with smaller volume in several temporal lobe regions. This is an observational study of emotional and brain changes and does not test any treatment, cure, or prevention.
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The results underscore the importance of reducing the number of cardiovascular risk factors for maintaining CBF and cognition in an aging population.
Why it matters
In 69 cognitively healthy late middle-aged adults, those with metabolic syndrome had about 15% lower gray matter cerebral blood flow and lower immediate memory, with blood flow partly explaining the memory difference. This is an observational study, so it does not show that treating metabolic syndrome prevents memory decline or dementia.
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Glial proliferation and activation are associated with disease progression in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar dementia.
Why it matters
Astrocytes made from human induced pluripotent stem cells carrying an ALS-causing TDP-43 mutation showed increased TDP-43, mislocalization and decreased survival, but did not harm cocultured motor neurons. This is a cell-culture study and does not test any treatment or prevention.
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51/100
The pattern of regional decreased cortical thickness that relates to cognitive deterioration is present in PD-MCI patients, involving areas that play a central role in the storage of prior experiences, integration of external perceptions, and semantic processing.
Why it matters
In 72 people with Parkinson's disease, this study found a pattern of progressive cortical thinning across stages from normal cognition to mild cognitive impairment to dementia, in areas involved in memory and other functions. It is a structural imaging study in Parkinson's disease and tests no treatment for Alzheimer's.
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Mutations in the glucocerebrosidase (GBA) gene, which encodes the lysosomal enzyme that is deficient in Gaucher's disease, are important and common risk factors for Parkinson's disease and related disorders.
Why it matters
This review reports that GBA mutations are common risk factors for Parkinson's disease and related Lewy body disorders, with carriers tending to have earlier onset and more cognitive changes. It discusses possible mechanisms but presents no treatment or cure.
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Early stages of many neurodegenerative diseases, such as Alzheimer's disease, vascular and frontotemporal dementia, and Parkinson's disease, are frequently associated with Mild Cognitive Impairment (MCI).
Why it matters
Pairs of brain-enriched plasma microRNA differentiated patients with mild cognitive impairment from age-matched controls, and in a separate longitudinal study detected mild cognitive impairment in most patients 1-5 years before clinical diagnosis. The authors say further testing in a larger study is necessary for validation of these results.
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Frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP) is a fatal neurodegenerative disease with no available treatments.
Why it matters
This study shows that TMEM106B is expressed in neurons in postmortem human brain tissue and that its expression is increased in FTLD-TDP brain, and it examines regulation by the microRNA-132/212 cluster and effects on progranulin pathways. It is laboratory research into frontotemporal dementia biology and does not provide a treatment, cure, or prevention.
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Patients with high likelihood DLB typically have normal hippocampal volumes but have atrophy in the dorsal mesopontine GM nuclei.
Why it matters
This study compared MRI brain measurements taken before death with autopsy findings in people who had Lewy body pathology. It found that hippocampus and amygdala volumes increased and dorsal mesopontine gray matter volumes decreased from low to high likelihood of dementia with Lewy bodies, which may help distinguish this condition but does not test treatment.
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Aggregation of the microtubule associated protein Tau is associated with several neurodegenerative disorders, including Alzheimer disease and frontotemporal dementia.
Why it matters
In cell cultures, tau fibrils released from one cell were taken up by others and triggered tau aggregation through direct protein contact, and an anti-tau antibody blocked this spread. This is laboratory work supporting a model of tau spreading and a possible vaccine approach, but it is not a treatment shown to work in patients.
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Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are part of a disease spectrum associated with TDP-43 pathology.
Why it matters
This paper describes the clinical and neuropathologic heterogeneity of c9FTD/ALS associated with the C9ORF72 hexanucleotide repeat expansion, noting that TDP-43 pathology in these cases was previously assumed to be uniform. It is a descriptive study and does not report any treatment, cure, or prevention.
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Loss of cholinergic neurons is associated with impaired cognitive function, particularly memory loss and Alzheimer disease (AD).
Why it matters
In this community-based cohort of nondemented people, higher concurrent dietary choline intake was associated with better verbal and visual memory performance. This is an observational association and does not show that choline intake prevents or treats Alzheimer's disease.
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Parkinson's disease (PD) is a common motor disorder of mysterious etiology.
Why it matters
This review discusses the genetic basis of Parkinson's disease, noting that genetic factors contribute to its complex pathogenesis. Over the past decade, more than 16 loci and 11 associated genes have been investigated for rare forms with Mendelian inheritance, representing no more than 10% of cases.
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Parkinson disease (PD) is progressive, with dementia and medication-refractory motor problems common reasons for late-stage nursing-home placement.
Why it matters
Evidence from animal models and human studies suggests ongoing vigorous exercise may favorably influence Parkinson disease progression, and midlife exercise significantly reduces later risk of dementia and mild cognitive impairment in seniors generally. No studies have addressed whether exercise influences dementia risk specifically in Parkinson disease.
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This prospective observational study included 22 patients with PCA who underwent CSF biomarker analysis of total tau (t-tau), phosphorylated tau on amino acid 181 (p-tau181), and amyloid β (Aβ(42)).
Why it matters
This study described cerebrospinal fluid biomarker profiles in 22 patients with posterior cortical atrophy and compared them to patients with typical Alzheimer's disease and other dementias. It is a small observational study and does not test any treatment, cure, or prevention.
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Type 2 diabetes is a risk factor for Alzheimer's disease, most likely linked to an impairment of insulin signaling in the brain.
Why it matters
In a mouse model of Alzheimer's disease, the diabetes drug liraglutide was tested after being shown to cross the blood-brain barrier. This is animal work only and reports no treatment, cure or prevention for people.
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Computational anatomy methods are now widely used in clinical neuroimaging to map the profile of disease effects on the brain and its clinical correlates.
Why it matters
This imaging study of up to 804 participants found that a new multivariate surface statistic detected localized hippocampal and ventricular differences associated with Alzheimer's disease and mild cognitive impairment with better effect sizes than conventional methods. The work is about improving brain imaging measures as candidate biomarkers for drug trials, not about treating, curing or preventing the disease.
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The association of rs1990622 with AAO explains, in part, the wide range in the AAO of disease among GRN mutation carriers.
Why it matters
In this study of granulin mutation carriers, the risk allele of rs1990622 (TMEM106B) was associated with a mean decrease in age at onset of 13 years and with lower plasma granulin levels in both healthy older adults and mutation carriers. This concerns a genetic modifier of disease onset in families with frontotemporal lobar degeneration, not a treatment, cure, or prevention for Alzheimer's disease.
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51/100
Niemann-Pick disease type C (NPC) is an inherited disorder characterized by intracellular accumulation of lipids such as cholesterol and glycosphingolipids in endosomes and lysosomes.
Why it matters
This cross-sectional study assessed whether altered lipid constituents in neuronal membranes affect amyloidogenic processing in Niemann-Pick disease type C, a disorder that shares some features with Alzheimer's disease but generally lacks amyloid-β plaques. It is an observational study of a different inherited disorder and does not test any 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.
- Impact of TREM2 risk variants on brain region-specific immune activation and plaque microenvironment in Alzheimer's disease patient brain samples
- TREM2 in Neurodegenerative Diseases
- The Alzheimer's disease-associated protective Plcγ2-P522R variant promotes immune functions
- Therapeutics for mitochondrial dysfunction-linked diseases in Down syndrome
- Mutations in FUS, an RNA Processing Protein, Cause Familial Amyotrophic Lateral Sclerosis Type 6
- Repeat expansion diseases
- TREM2 - a key player in microglial biology and Alzheimer disease
- Focused Ultrasound-mediated Liquid Biopsy in a Tauopathy Mouse Model
- Non-Fluent Speech in Frontotemporal Lobar Degeneration
- Common variants at 12q14 and 12q24 are associated with hippocampal volume