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.
-
The protein triggering receptor expressed on myeloid cells-2 (TREM2) is an immunomodulatory receptor with a central role in myeloid cell activation and survival.
Why it matters
This 2017 review starts from background it summarises: TREM2 coding variants "increase risk for Alzheimer's disease and other neurodegenerative diseases", and animal studies point to TREM2's importance in models including COPD, multiple sclerosis and stroke. Its focus is an open question: TREM2's mechanism "remains elusive", in part because the identity of its natural binding partners (ligands) is not conclusively known, and the many ligands proposed have a "physiological role and mechanism of engagement" that "remain to be determined". The record reports no new data and no named ligand, and it tests no treatment.
-
The clinical progression of Alzheimer disease (AD) is associated with the accumulation of tau neurofibrillary tangles, which may spread throughout the cortex by interneuronal tau transfer.
Why it matters
This in vitro study tested a panel of tau antibodies for their ability to block neuronal uptake and aggregation of tau, with the idea that targeting extracellular tau might slow the spread of tau pathology. It is early laboratory work and does not test any treatment, cure, or prevention in people.
-
Previously, the contribution of peripheral infection to cognitive decline was largely overlooked however, the past 15 years have established a key role for infectious pathogens in the progression of age-related neurodegeneration.
Why it matters
This review states that the brain's immune privilege is not absolute and that Alzheimer's patients are more vulnerable to infection-related cognitive changes. It suggests that peripheral infection and inflammation matter for disease progression, but reports no treatment or cure.
-
Progranulin (PGRN) is implicated in Alzheimer's disease (AD) as well as frontotemporal lobar degeneration.
Why it matters
This study found that the GRN Alzheimer's disease risk variant had no significant effects on amyloid imaging or cerebrospinal fluid Aβ levels, whereas it was associated with increased cerebrospinal fluid tau. It is an observational genetic and biomarker analysis and does not report any treatment, cure, or prevention for Alzheimer's disease.
-
The importance of (micro)vascular contributions to cognitive impairment and dementia (VCID) in aging cannot be overemphasized, and the pathogenesis and prevention of age-related cerebromicrovascular pathologies are a subject of intensive research.
Why it matters
This review describes how aging impairs neurovascular coupling and how astrocyte dysfunction and endothelial impairment may contribute to cognitive decline. It reports no treatment, cure or prevention tested in patients.
-
Study objectives Emerging evidence suggests a role for sleep in contributing to the progression of Alzheimer disease (AD).
Why it matters
In cognitively normal older adults, less slow-wave sleep was linked to higher levels of the amyloid-related protein Aβ42 in spinal fluid. This suggests disturbed sleep might raise soluble brain amyloid before plaques form, but it does not show that improving sleep prevents Alzheimer's disease.
-
Regeneration of injured nerves is likely occurring in the peripheral nervous system, but not in the central nervous system.
Why it matters
This is a rat-model analysis of gene expression after sciatic nerve injury, focused on non-coding RNAs and neuropathic pain. It provides no information about treating, curing or preventing Alzheimer's disease.
-
Early-phase FBB acquisitions correlate on a relative quantitative and visual level with FDG PET scans, irrespective of the amyloid plaque density assessed in late FBB imaging.
-
48/100
Neuropathic pain afflicts millions of people, and the development of an effective treatment for this intractable pain is an urgent issue.
Why it matters
In mice, TREM2/DAP12 signaling in microglia promoted inflammation and worsened neuropathic pain, and blocking it reduced pain behaviors. This is about pain after nerve injury in mice, not Alzheimer's disease.
-
Immunotherapeutic approaches are currently the most advanced treatments for Alzheimer's disease (AD).
Why it matters
This study found that loss of TREM2 reduces the ability of microglia to clear amyloid plaques after antibody treatment. It is experimental work on how immunotherapy may work and does not establish a treatment, cure or prevention for people.
-
Our findings suggest that the proposition that synaptic markers can predict cognitive decline in AD, should be extended to Lewy body diseases.
-
Mutations in triggering receptor expressed on myeloid cells 2 (TREM2), which has been proposed to regulate the inflammatory responses and the clearance of apoptotic neurons and/or amyloid-β, are genetically linked to increased risk for late-onset Alzheimer's disease (AD).
Why it matters
TREM2 is a known Alzheimer's risk gene, and a variant in its neighbour TREML2 has been reported to protect against the disease. In mice, this study found that an inflammatory trigger (LPS) "significantly suppressed TREM2 but increased TREML2 expression" in the brain, and that LPS or amyloid-β oligomers did the same in microglia grown in a dish. These are expression changes in mouse models, not human results, and they do not point to any treatment.
-
Neurodegeneration is a phenomenon that occurs in the central nervous system through the hallmarks associating the loss of neuronal structure and function.
Why it matters
This review states that causative agents of neurodegeneration have yet to be identified but that recent data link the inflammatory process closely with multiple neurodegenerative pathways. It discusses neuroinflammation in diseases including Alzheimer's disease and reports no treatment, cure or prevention.
-
48/100
Despite the significant impact of postoperative delirium on surgical outcomes and the long-term prognosis of older patients, its neural basis has not yet been clarified.
-
Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis with associated frontotemporal dementia (ALS/FTD) are major neurodegenerative diseases for which there are no cures.
Why it matters
This review discusses evidence that disturbances in contacts between the endoplasmic reticulum and mitochondria occur in Alzheimer's disease, Parkinson's disease, and ALS/FTD. It raises the question of which damaged function to target for therapy but reports no treatment or cure.
-
48/100
As a novel risk gene for Alzheimer's disease (AD), triggering receptor expressed on myeloid cells 2 (TREM2) gene encodes a type I transmembrane receptor that is uniquely expressed by the microglia in the brain.
Why it matters
In P301S mice, a model of tau pathology, the authors report that brain TREM2 "was upregulated … during disease progression", and their earlier work found that silencing microglial TREM2 "exacerbated spatial cognitive deficits and tau pathology". The paper's title says TREM2 "provides neuroprotection" in these mice, but the summary we hold ends before its methods and results, so we cannot show what was measured or how large the effect was. These are mouse findings and do not establish a treatment, cure or prevention for people.
-
Currently there are no effective treatments for many neurodegenerative diseases.
Why it matters
This work used a proteomic profiling method to search for new cerebrospinal fluid markers that could help tell Lewy Body Dementia apart from other dementias such as Alzheimer's disease. It is a biomarker discovery study and does not test any treatment, cure, or prevention.
-
Inflammasomes are high molecular weight protein complexes that assemble in the cytosol upon pathogen encounter.
Why it matters
This laboratory study in mouse cells identified NEK7 as a needed component for activation of the Nlrp3 inflammasome, a process that has been implicated in Alzheimer's disease and other conditions. It is early, cell-based work and does not test any treatment in people.
-
Tau pathology is a pathological hallmark for several neurodegenerative diseases including Alzheimer's disease and frontotemporal dementia.
Why it matters
In P301S tau mice, silencing TREM2 worsened tau pathology, neurodegenerative changes, and spatial learning deficits. This is animal work and does not establish a treatment or prevention for Alzheimer's disease in people.
-
Previous studies demonstrate that intrastriatal injections of fibrillar alpha-synuclein (α-syn) into mice induce Parkinson's disease (PD)-like Lewy body (LB) pathology formed by aggregated α-syn in anatomically interconnected regions and significant nigrostriatal degeneration.
Why it matters
In rats, intrastriatal injection of mouse alpha-synuclein pre-formed fibrils produced Lewy body-like inclusions in several brain regions and nigrostriatal degeneration. This is an animal model study of Parkinson's disease-like pathology and reports no treatment, cure, or prevention.
-
Repetitive brain trauma is associated with a progressive neurological deterioration, now termed as chronic traumatic encephalopathy (CTE).
Why it matters
This review describes chronic traumatic encephalopathy as a tauopathy linked to repetitive brain trauma, with symptoms that can include memory loss, cognitive impairment and dementia, and notes it can only be diagnosed with certainty by neuropathological examination. It states that identifying genetic risk factors and understanding how other variables contribute to its development is critical.
-
Alzheimer's disease (AD) is characterized by a robust inflammatory response elicited by the accumulation and subsequent deposition of amyloid (Aβ) within the brain.
Why it matters
In mouse models of Alzheimer's, treating myeloid cells with nuclear receptor agonists increased phagocytosis-related genes and enhanced clearance of amyloid plaques. This is animal research and does not establish a treatment for people.
-
Neuronal active Caspase-6 (Casp6) is associated with Alzheimer disease (AD), cognitive impairment, and axonal degeneration.
Why it matters
In cultured human neurons, the NLRP1 inflammasome was found to activate Caspase-1 and Caspase-6. This is laboratory cell research and does not show any treatment or prevention for Alzheimer's disease.
-
Elevation of both neuronal iron and nitric oxide (NO) in the substantia nigra are associated with Parkinson's disease (PD) pathogenesis.
Why it matters
This work links loss of amyloid precursor protein to iron accumulation and cell loss in Parkinson's disease, not Alzheimer's disease. It does not provide evidence for treating, curing or preventing Alzheimer's disease.
-
The key role of APP in the pathogenesis of Alzheimer disease is well established.
Why it matters
Mice that lack both APP and its relative APLP2 die soon after birth, so until this study nobody could see what these Alzheimer's-linked proteins normally do in the adult brain. By removing both genes only in excitatory forebrain neurons, the researchers found that adult mice had "pronounced deficits in the induction and maintenance of hippocampal LTP", a lab measure of how nerve-cell connections strengthen, along with signs of "a possible presynaptic deficit." This is mouse research. It suggests APP-family proteins matter for normal synapse function, but it does not test any treatment in people.
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.
- Quantification of Lewy body pathology by cerebrospinal fluid endpoint dilution RT-QuIC in a neuropathological autopsy cohort of clinically heterogeneous participants
- Ammonia induced decrease in glial fibrillary acidic protein in cultured astrocytes
- Neocortical cholinergic neurons in elderly people
- Changes of a Cerebral Cavernous Malformation Associated With Lecanemab Therapy in a Patient With Alzheimer Disease
- Dystrophic microglia are associated with neurodegenerative disease and not healthy aging in the human brain
- Role of nitric oxide in inflammation-mediated neurodegeneration
- Serum neuronal exosomes predict and differentiate Parkinson's disease from atypical parkinsonism
- Vascular Smooth Muscle Cell Dysfunction in Cerebral Small Vessel Disease: Mechanisms and Therapeutic Potential
- Cerebral FURIN deficiency impairs astrocytic lipophagy through ITGAV maturation
- Inhaled xenon modulates microglia and ameliorates disease in mouse models of amyloidosis and tauopathy