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.
-
Patients with autopsy-confirmed low-, intermediate-, and high-likelihood DLB, according to the probability statement recommended by the third report of the DLB Consortium, and antemortem MRI, were identified (n = 75).
Why it matters
In people with dementia with Lewy bodies, having probable REM sleep behavior disorder was linked to a higher likelihood of that diagnosis and to less severe Alzheimer-related brain changes in the hippocampus and amygdala. This is an autopsy study of 75 patients and does not test any treatment, so it does not show how to cure or prevent Alzheimer's disease.
-
Delayed neuronal loss and brain atrophy after cerebral ischemia contribute to stroke and dementia pathology, but the mechanisms are poorly understood.
Why it matters
In this study, blocking phagocytosis prevented delayed loss and death of functional neurons after transient brain ischemia in mice, and deficiency in either of two phagocytic proteins was protective. This is animal research on stroke-related neuronal death, not a demonstrated Alzheimer's treatment.
-
An increasingly popular method of assessing cognitive functions in rodents is the automated touchscreen platform, on which a number of different cognitive tests can be run in a manner very similar to touchscreen methods currently used to test human subjects.
Why it matters
This protocol describes how to run four touchscreen learning and memory assays in rats and mice, which can be used to study rodent models of neurodegenerative diseases including Alzheimer's disease. It is a research method and reports no treatment, cure, or prevention.
-
50/100
Triggering receptor expressed on myeloid cells 2 (TREM2) homozygous mutations cause Nasu-Hakola disease, an early-onset recessive form of dementia preceded by bone cysts and fractures.
Why it matters
TREM2 mutations were already known to cause Nasu-Hakola disease, an early-onset dementia preceded by bone cysts and fractures, and had recently been reported in frontotemporal dementia without bone problems. This 2013 report describes one Turkish family with a frontotemporal dementia-like illness carrying two different TREM2 mutations (compound heterozygous), which the authors call the first such case and say "further confirm[s]" the TREM2 link to FTD-like illness. The stored abstract does not name the mutations or say how many relatives were affected, and it does not concern Alzheimer's disease or any treatment.
-
Several recent breakthroughs have provided notable insights into the pathogenesis of amyotrophic lateral sclerosis (ALS), with some even shifting our thinking about this neurodegenerative disease and raising the question as to whether this disorder is a proteinopathy, a ribonucleopathy or both.
Why it matters
This review summarizes recent findings on the causes of ALS and notes mechanistic links between ALS and frontotemporal dementia and other neurodegenerative diseases. It discusses what these findings teach about the disease and what questions remain, but it does not report a treatment or cure.
-
Human apolipoprotein E (apoE) isoforms may differentially modulate amyloid-β (Aβ) levels.
Why it matters
Using a new ELISA, this study found lower soluble apoE/Aβ complex levels and higher oligomeric Aβ with APOE4 and in Alzheimer's disease, in a transgenic mouse model and in human samples. This is laboratory and sample-based work that suggests a mechanism, not a treatment, cure, or prevention for Alzheimer's disease.
-
50/100
Progranulin (PGRN) is a widely expressed secreted protein that is linked to inflammation.
Why it matters
Mice lacking progranulin, which is linked to frontotemporal dementia in humans, lost more neurons after a toxin injury. This is animal research and does not show a treatment or cure for dementia in people.
-
50/100
Alzheimer's disease (AD) is the most common progressive neurodegenerative disorder causing dementia.
Why it matters
This laboratory study found that apoE, especially apoE4, increases the formation of amyloid beta oligomers, and that APOE ε4/ε4 AD patient brains had higher levels of these oligomers than APOE ε3/ε3 brains. It identifies a possible mechanism linking a genetic risk factor to amyloid beta oligomerization but does not test any treatment, cure, or prevention.
-
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease of motor neurons leading to death from respiratory failure within about 3 years of symptom onset.
Why it matters
This review describes genes linked to ALS, including SOD1, TARDBP and FUS, and notes that some cases overlap with frontotemporal dementia. It does not report any treatment, cure or prevention for Alzheimer's disease.
-
50/100
Microstructural white matter changes are present in cognitively normal individuals in the pre-aMCI stage, and may serve as a potential imaging marker of early AD-related brain changes.
Why it matters
Among 193 cognitively normal people, the 20 who developed amnestic mild cognitive impairment two years later already had reduced white matter integrity in the precuneus, parahippocampal cingulum, parahippocampal gyrus white matter and fornix at baseline, while gray matter was relatively intact. This identifies early imaging markers of risk but does not test any treatment, cure or prevention.
-
Type 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer disease (AD).
Why it matters
In a small comparison of 10 people with type 2 diabetes and 11 controls, the diabetes group showed reduced resting-state functional connectivity in the default mode network, with no group differences in cognition or hippocampal size. The sample is very small, and the study does not show that treating diabetes prevents Alzheimer disease.
-
Neuroinflammation is associated with virtually all major neurodegenerative disorders, including Alzheimer's disease (AD).
Why it matters
This study found that the TNF-α synthesis inhibitor 3,6'-dithiothalidomide reduced markers of inflammation, Alzheimer pathology, and behavioral deficits in cellular and rodent models. It is animal and cell research and does not establish that this drug treats or prevents Alzheimer's disease in people.
-
TREM2 is an immunoreceptor expressed on osteoclasts (OC) and microglia that transmits intracellular signals through the adaptor DAP12.
Why it matters
Mice bred without the TREM2 gene had thinner, lower-density bones ("an osteopenic phenotype reminiscent of NHD"), the bone side of Nasu-Hakola disease, an inherited condition that causes bone cysts and early dementia. In lab-dish experiments, cells that become osteoclasts (bone-removing cells) divided less and switched on less β-catenin when they lacked TREM2. This is a mouse and cell study of bone with no brain or Alzheimer's findings, and it tests no treatment.
-
These data weakly corroborate prior findings of associations between LTL and mortality in the elderly.
-
50/100
Genotyping of patients is useful to confirm the diagnosis in the latter patients and essential for future prenatal diagnosis.
Why it matters
This review discusses Niemann-Pick disease type C, a different disorder, and mentions a treatment for its neurological manifestations. It does not address Alzheimer's disease treatment, cure, or prevention.
-
50/100
Hippocampal volume shrinks in late adulthood, but the neuromolecular factors that trigger hippocampal decay in aging humans remains a matter of speculation.
Why it matters
This study tested whether age-related reductions in serum levels of brain-derived neurotrophic factor are related to shrinkage of the hippocampus and memory deficits in older adults. In rodents, BDNF promotes growth and proliferation of cells in the hippocampus and is important in long-term potentiation and memory formation.
-
Cerebral ischemic small vessel disease (SVD) is the leading cause of vascular dementia and a major contributor to stroke in humans.
Why it matters
A mouse model carrying a CADASIL-causing Notch3 mutation reproduced vessel deposits, progressive white matter damage and reduced cerebral blood flow, with cerebrovascular dysfunction appearing before white matter lesions. This is an animal model of a vascular small vessel disease and does not test any treatment or prevention for Alzheimer's disease.
-
50/100
TDP-43 has been found in inclusion bodies of multiple neurological disorders, including amyotrophic lateral sclerosis, frontotemporal dementia, Parkinson's disease and Alzheimer's disease.
Why it matters
In cell lines, primary motor neurons, and zebrafish embryos, three TARDBP mutations caused motor neuron defects and toxicity, with evidence for both toxic gain of function and loss of function. This laboratory work suggests how mutant TDP-43 may contribute to disease but reports no treatment, cure, or prevention.
-
Type 2 diabetes, cardiovascular diseases, colon cancer, breast cancer, dementia and depression constitute a cluster of diseases, which defines 'a diseasome of physical inactivity'.
Why it matters
This paper proposes that physical inactivity and abdominal fat are linked to a group of diseases including dementia, and suggests that exercise may protect partly through anti-inflammatory effects. The ideas about myokines and inflammation are presented as a theory, not as proven treatment or prevention for Alzheimer's disease.
-
Amyotrophic lateral sclerosis (ALS) is increasingly recognized to be a multisystem disorder which includes both clinical and neuropathological features of a frontotemporal lobar degeneration (FTLD).
Why it matters
This consensus paper addresses the need for a common framework to discuss the cognitive and behavioural syndromes of amyotrophic lateral sclerosis, which is increasingly recognized to include features of frontotemporal lobar degeneration. The recommendations define clinical diagnosis of the underlying motor neuron disease, cognitive and behavioural dysfunction, additional non-motor manifestations, and disease modifiers.
-
The adoption into the UK of children who have been reared in severely deprived conditions provides an opportunity to study possible association between very early negative experiences and subsequent brain development.
-
There are no conventional lymphatics in the brain but physiological studies have revealed a substantial and immunologically significant lymphatic drainage from brain to cervical lymph nodes.
Why it matters
This review discusses lymphatic drainage of the brain and its relevance to neurological disease. It notes that cerebrospinal fluid drains via the cribriform plate and nasal mucosa to cervical lymph nodes, and that lymphatic drainage of interstitial fluid and solutes from brain parenchyma occurs along capillary and artery walls.
-
TAR DNA-binding protein (TDP-43) has been recently described as a major pathological protein in both frontotemporal dementia with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis.
Why it matters
This laboratory study used new antibodies to analyze different forms of TDP-43 protein in brain and spinal cord tissue from people with frontotemporal lobar degeneration and ALS. It concerns those diseases, not Alzheimer's disease, and does not test any treatment, cure, or prevention for Alzheimer's.
-
Cardiac 123I-MIBG findings are similar among idiopathic RBD and the syndromes of PD and DLB, but differ from those of PSP and MSA.
-
The presence of abnormal TDP-43 immunoreactivity is associated with a modified Alzheimer disease clinicopathologic and radiologic phenotype.
Why it matters
Among 84 people with confirmed Alzheimer's pathology, 34% also had abnormal TDP-43 immunoreactivity, and those people were older and performed worse on cognitive tests. This is a postmortem and imaging study that describes a subtype of Alzheimer's but does not test any treatment or show that targeting TDP-43 would help.
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.
- Trans-cellular propagation of Tau aggregation by fibrillar species
- Alkalizing drugs induce accumulation of amyloid precursor protein by-products in luminal vesicles of multivesicular bodies
- Source-based morphometry: the use of independent component analysis to identify gray matter differences with application to schizophrenia
- Morphological and biochemical assessment of DNA damage and apoptosis in Down syndrome and Alzheimer disease, and effect of postmortem tissue archival on TUNEL
- Monomeric C-reactive protein--a key molecule driving development of Alzheimer's disease associated with brain ischaemia?
- Partial BACE1 reduction in a Down syndrome mouse model blocks Alzheimer-related endosomal anomalies and cholinergic neurodegeneration: role of APP-CTF
- Frontotemporal dementia and Parkinsonism linked to chromosome 17: a new group of tauopathies
- Increased expression of BIN1 mediates Alzheimer genetic risk by modulating tau pathology
- p75 neurotrophin receptor modulation in mild to moderate Alzheimer disease: a randomized, placebo-controlled phase 2a trial
- Amyloid Oligomers Exacerbate Tau Pathology in a Mouse Model of Tauopathy