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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48/100
Moreover, we found, in either the whole AD population or both subgroups, a CSF profile in which higher
Why it matters
In 145 drug-naive patients with Alzheimer's disease, this study correlated cerebrospinal fluid lactate levels with tau proteins, beta-amyloid and Mini-Mental State Examination scores. It describes a biological relationship in the disease but does not test a treatment, cure or prevention.
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The blood-brain barrier (BBB) is a tightly regulated interface in the Central Nervous System (CNS) that regulates the exchange of molecules in and out from the brain thus maintaining the CNS homeostasis.
Why it matters
This review describes how astrocytes help form and maintain the blood-brain barrier, and notes that this barrier is disrupted in neurological disorders including Alzheimer's and Parkinson's diseases. It reports no treatment or prevention finding, only a possible disease mechanism.
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Immunotherapeutic approaches are currently in the spotlight for their potential as disease-modifying treatments for neurodegenerative disorders.
Why it matters
This paper describes a next-generation active vaccination approach using short AFFITOPE peptides for synucleinopathies such as Parkinson's disease. It concerns Parkinson's disease immunization and reports no Alzheimer's disease treatment, cure or prevention.
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Hippocampal T2 hyperintensity after FSE represents acute injury often evolving to a radiological appearance of HS after 1 year.
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Alzheimer's disease (AD) is the leading cause of dementia and has no cure.
Why it matters
In an Alzheimer's disease mouse model, inhibiting ROCK2 with a small molecule reduced amyloid-β production by affecting BACE1 and APP processing. ROCK2 protein levels were increased in human Alzheimer's, mild cognitive impairment and asymptomatic Alzheimer's brain, but this is early animal and cell work, not a proven treatment.
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Aggregates of hyperphosphorylated tau (PHF-tau), such as neurofibrillary tangles, are linked to the degree of cognitive impairment in Alzheimer's disease.
Why it matters
Describes the first human brain images with [F18]-T808, a new PET imaging agent that targets tau aggregates such as neurofibrillary tangles, which are linked to the degree of cognitive impairment in Alzheimer's disease.
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Triggering receptor expressed on myeloid cells-2 (TREM2) and its signaling adaptor protein TYROBP/DAP12 play important roles in signal transduction in dendritic cells, osteoclasts, tissue macrophages, and microglia.
Why it matters
TREM2 is a receptor on immune cells, including the brain's microglia, and variants in its gene have been linked to late-onset Alzheimer's disease. This laboratory study reports that TREM2 is cut in two steps: its outer part is first shed from the cell surface, and the stub left in the membrane is then cut by the enzyme γ-secretase. When γ-secretase was blocked by a drug or genetically, the stub built up at the cell surface and still bound its signalling partner DAP12; the study tested no treatment and did not study patients.
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Hypothalamic-pituitary-adrenal axis hyperresponsiveness and a less frequent suppression of the GH/IGF-1 axis in response to acute stress are possibly involved in delirium pathophysiology.
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48/100
The interstitial fluid (ISF) drainage pathway has been hypothesized to underlie the clearance of solutes and metabolites from the brain.
Why it matters
Scientists had long suspected that fluid drains out of the brain along the spaces around arteries, but the authors note this "has never been demonstrated directly". They built a new way to watch this drainage in real time in living mice, and report that it was impaired in mouse models of ischemic stroke and Alzheimer's disease, a route thought to help clear amyloid beta. This is animal research: it does not show that the same happens in people, and it does not test any treatment.
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Aggregates of hyperphosphorylated tau (PHF-tau), such as neurofibrillary tangles, are linked to the degree of cognitive impairment in Alzheimer's disease.
Why it matters
The authors describe the first human brain images with [F-18]-T807, a PET imaging agent they developed to target aggregated tau (PHF-tau). They say it may be useful for imaging Alzheimer's disease and other tauopathies.
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Enlarged perivascular spaces are associated with age, lacunar stroke subtype and white matter lesions and should be considered as another magnetic resonance imaging marker of cerebral small vessel disease.
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Accumulation of tau is a critical event in several neurodegenerative disorders, collectively known as tauopathies, which include Alzheimer's disease and frontotemporal dementia.
Why it matters
In animal models, increasing mTOR signaling raised tau levels and phosphorylation, while reducing it with rapamycin improved tau pathology and behavior in mice overexpressing mutant human tau. The authors present this as preclinical evidence that reducing mTOR signaling may be a valid therapeutic approach for tauopathies, not a proven treatment.
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Cerebrovascular disease has an important role in cognitive decline and dementia.
Why it matters
This study found that small cortical microinfarcts, previously undetectable in living people, could be seen on high-resolution 7T MRI and were confirmed on postmortem tissue in some cases. It is a detection method for vascular brain lesions and does not test any treatment, cure, or prevention for Alzheimer disease.
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APOE affects microstructural properties of the brain WM from early adulthood, but the specific allelic effects do not directly reflect the associated risk of developing Alzheimer disease.
Why it matters
Healthy adults carrying the APOE ε3/ε4 genotype showed widespread differences in brain white matter microstructure compared with ε3/ε3 carriers, and these differences appeared stable from early adulthood. This suggests APOE may affect brain structure long before any dementia symptoms, but it does not show that these changes cause Alzheimer disease.
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TDP-43 is a multifunctional DNA/RNA-binding protein that has been identified as the major component of the cytoplasmic ubiquitin (+) inclusions (UBIs) in diseased cells of frontotemporal lobar dementia (FTLD-U) and amyotrophic lateral sclerosis (ALS).
Why it matters
In a mouse model of TDP-43 proteinopathy, rapamycin and other autophagy activators rescued learning and memory impairment and slowed motor decline. This is an animal 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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The β-site amyloid precursor protein-cleaving enzyme BACE1 is a prime drug target for Alzheimer disease.
Why it matters
Using a proteomic approach on the secretions of primary neurons after acute BACE1 inhibition, this study identified the adhesion molecules L1 and CHL1 as new substrates cleaved by BACE1 in vivo. This raises questions about the safety of BACE1 as a drug target but does not itself demonstrate any treatment or cure.
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The histopathological hallmark of Parkinson's disease (PD) is the presence of fibrillar aggregates referred to as Lewy bodies (LBs), in which α-synuclein is a major constituent.
Why it matters
This review reports that recent studies indicate nonfibrillar alpha-synuclein is cytotoxic and that fibrillar aggregates such as Lewy bodies and pale bodies may represent a cytoprotective mechanism in Parkinson's disease. It offers no tested treatment, cure, or prevention.
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Although epidemiological data associate hypertension with a strong predisposition to develop Alzheimer disease, no mechanistic explanation exists so far.
Why it matters
This study in mice found that hypertension led to amyloid plaques, neuroinflammation, blood-brain barrier dysfunction, and cognitive impairment through activation of RAGE in brain blood vessels. This is animal research and does not yet show whether treating hypertension or targeting RAGE would prevent or treat Alzheimer's disease in people.
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Olfactory dysfunction is among the earliest nonmotor features of Parkinson disease (PD).
Why it matters
This review describes smell loss as an early feature of Parkinson disease that can appear years before motor symptoms, and notes that equivalent deficits are seen in Alzheimer disease. It suggests that loss of smell may share a common pathological basis across these diseases and could help tell them apart from other disorders, but the mechanisms behind it remain unknown.
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One of the pathological hallmarks of Alzheimer disease is the accumulation of amyloid plaques in the extracellular space in the brain.
Why it matters
In cell and mouse experiments, reducing PICALM lowered APP internalization and amyloid-beta production, while increasing PICALM raised them, and knocking down PICALM in mice reduced amyloid plaques. This is early laboratory work identifying a possible mechanism linking the PICALM gene to amyloid plaque formation.
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Although aberrant microRNA (miRNA) expression is linked to human diseases including cancer, the mechanisms that regulate the expression of each individual miRNA remain largely unknown.
Why it matters
This laboratory work found that TDP-43 helps produce certain microRNAs in cells and that this role is needed for neurons to grow. It is early, cell-based research, so it does not yet show any treatment, cure or prevention for Alzheimer's disease.
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Autosomal dominant cerebellar ataxia, deafness and narcolepsy (ADCA-DN) is characterized by late onset (30-40 years old) cerebellar ataxia, sensory neuronal deafness, narcolepsy-cataplexy and dementia.
Why it matters
This study identified mutations in DNMT1 in families with autosomal dominant cerebellar ataxia, deafness and narcolepsy, a condition that includes dementia. It reports no treatment, cure or prevention for Alzheimer's disease.
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While cognitive deficits are increasingly recognized as common symptoms in amyotrophic lateral sclerosis (ALS), the underlying histopathologic basis for this is not known, nor has the relevance of neuroinflammatory mechanisms and microglial activation to cognitive impairment (CI) in ALS been systematically analyzed.
Why it matters
This study examined brain tissue from 102 autopsy cases of amyotrophic lateral sclerosis and related microglial activation and TDP-43 pathology to cognitive measures. It is about the brain basis of cognitive problems in ALS and does not test any treatment, cure, or prevention for Alzheimer's disease.
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48/100
Amyloid β (Aβ) peptides are proteolytic products from amyloid precursor protein (APP) and are thought to play a role in Alzheimer disease (AD) pathogenesis.
Why it matters
In 25 patients resuscitated after cardiac arrest, serum amyloid beta 42 levels rose over time after hypoxia, using an ultrasensitive assay. This is a small human study of a possible trigger for amyloid buildup and reports no treatment, cure or prevention.
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Chronic traumatic encephalopathy (CTE) has been linked to participation in contact sports such as boxing and American football.
Why it matters
This paper describes chronic traumatic encephalopathy, linked to repetitive brain trauma in contact sports, as a condition that can eventually lead to dementia and is marked by accumulations of hyperphosphorylated tau and TDP-43 proteins. It calls for more study of risk factors and diagnosis to potentially allow prevention and treatment, but reports no current treatment or cure.
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.
- Antemortem α-Synuclein levels from neuron-derived extracellular vesicles identify Lewy Body pathology in Parkinson’s Disease and Alzheimer Disease
- Plasma extracellular vesicle tau and TDP-43 as diagnostic biomarkers in FTD and ALS
- Neuropathologic basis of white matter hyperintensity accumulation with advanced age
- Tandem repeats mediating genetic plasticity in health and disease
- [Quercetin ameliorates inflammation in CA1 hippocampal region in aged triple transgenic Alzheimer´s disease mice model.]
- CRISPR screens in iPSC-derived neurons reveal principles of tau proteostasis
- Arterial Spin-Labeling MRI Identifies Abnormal Perfusion Metric at the Gray Matter/CSF Interface in Cerebral Small Vessel Disease
- C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal trafficking
- Sex-specific modulation of amyloid-β on tau phosphorylation underlies faster tangle accumulation in females
- Trem2 promotes foamy macrophage lipid uptake and survival in atherosclerosis