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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There is a large body of evidence to suggest that improving periconceptional folate status reduces the risk of neonatal neural tube defects.
Why it matters
This review compares folic acid and L-5-methyltetrahydrofolate and notes growing evidence that folic acid may have a role in preventing diseases including dementia. It does not report any trial results on dementia outcomes, so it cannot show whether either form of folate prevents or treats Alzheimer's disease.
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Progranulin haploinsufficiency causes frontotemporal dementia with tau-negative, ubiquitin-positive neuronal inclusion pathology.
Why it matters
Progranulin-deficient mice displayed depression- and disinhibition-like behavior and deficits in social recognition from a young age, and 18-month-old mice showed impaired spatial learning and memory. This is a mouse model of frontotemporal dementia, so it does not establish a treatment, cure, or prevention for Alzheimer's disease.
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Obesity is a growing global health problem that contributes to diabetes, hypertension, cardiovascular diseases, dementia, and cancer.
Why it matters
In mice, seven weeks of a high-fat diet significantly decreased the number of newly generated cells in the hippocampus without neuronal loss, and increased lipid peroxidation while decreasing brain-derived neurotrophic factor. This is animal work indicating that a high-fat diet impairs hippocampal neurogenesis and neural progenitor cell proliferation.
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Vaccine-based autoimmune (anti-amyloid) treatments are currently being examined for their therapeutic potential in Alzheimer's disease.
Why it matters
In a transgenic mouse model of amyloid pathology, TREM2 and Tmem176b were highly expressed in plaque-associated microglia, defining two different zones of activation. The findings relate to vaccine-based anti-amyloid approaches but are animal work with no demonstrated therapy.
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Cerebrospinal fluid (CSF) measures of Ab and tau, Pittsburgh Compound B (PIB) imaging and hippocampal atrophy are promising Alzheimer's disease biomarkers yet the associations between them are not known.
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The abnormal enlargement of the amygdala and hippocampus in adolescents with autism adds to previous findings of enlargement of these structures in children with autism.
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Nerve growth factor (NGF)-dependent cholinergic basal forebrain neurons degenerate during the progression of Alzheimer disease (AD).
Why it matters
Higher MMP-9 activity was found in brain tissue from people with mild cognitive impairment and Alzheimer's disease compared with those with no cognitive impairment. This suggests that reduced mature nerve growth factor from MMP-9 degradation may contribute to the cognitive deficits seen in these conditions, though the study examined tissue samples and does not establish cause or a treatment.
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43/100
Presenilin 1(PS1) is the catalytic subunit of gamma-secretase, the enzyme responsible for the Abeta C-terminal cleavage site, which results in the production of Abeta peptides of various lengths.
Why it matters
This laboratory study used a FRET probe to test whether modulators of gamma-secretase act by allosterically changing presenilin structure in relation to the amyloid beta(42/40) ratio. It is basic molecular research and does not test any treatment, cure, or prevention in people.
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Hydrogen sulfide (H(2)S) is an essential physiological product in brain.
Why it matters
This laboratory study found that astrocytes produce hydrogen sulfide, described as an anti-inflammatory and neuroprotective agent, and that astrocytes had much higher synthesis than other cell types tested. It is early cell and tissue work and does not show any effect on treating or preventing Alzheimer's disease in people.
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Object Damage to axons contributes to postinjury disabilities and is commonly observed following traumatic brain injury (TBI).
Why it matters
This feasibility study used intracerebral microdialysis to collect interstitial total tau and amyloid beta 1-42 proteins in eight patients after moderate-to-severe traumatic brain injury. It is a small early feasibility study and does not test any treatment, cure, or prevention for Alzheimer disease.
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The incidence of obesity has increased dramatically during recent decades.
Why it matters
This review states that dysfunction of fat tissue in obesity may link obesity to several health problems, including dementia. It discusses a possible mechanism and does not test any treatment, cure or prevention for Alzheimer's disease.
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The amyloid precursor protein (APP) is implied both in cell growth and differentiation and in neurodegenerative processes in Alzheimer disease.
Why it matters
This laboratory study found that the neuroprotective secreted amyloid precursor protein acts by disrupting APP dimers. It describes a mechanism of APP signalling and does not test a treatment or prevention in people.
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43/100
The pattern of thinning in TLE-no was different from the pattern in TLE-MTS.
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There is emerging evidence from healthy individuals, as well as direct and indirect evidence from psychiatric and neurological patients with disease-related hippocampal atrophy, linking the cortisol awakening response (CAR) to hippocampal volume.
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Amyloid beta-peptide (Abeta) accumulation leads to neurodegeneration and Alzheimer disease; however, amyloid metabolism is a dynamic process and enzymic mechanisms exist for Abeta removal.
Why it matters
In two neuroblastoma cell lines, the amyloid precursor protein intracellular domain bound directly to the neprilysin promoter in high-expressing cells but not in low-expressing cells. This is a cell-based finding about amyloid removal and does not show that altering neprilysin treats or prevents Alzheimer's disease.
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The receptor for advanced glycation end products (RAGE) is a 55-kDa type I membrane glycoprotein of the immunoglobulin superfamily.
Why it matters
This study describes how the RAGE receptor is shed from cells by metalloproteinases, a process relevant to conditions including Alzheimer's disease. It is laboratory cell research and does not test any treatment or cure.
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Inclusion body myopathy (IBM) associated with Paget disease of the bone (PDB) and frontotemporal dementia (FTD) (now called IBMPFD), is a progressive autosomal dominant disorder that was recently identified as being caused by mutations in the VCP (p97 or CDC48) gene which plays a key role in the ubiquitin-proteasome dependent degradation of cytosolic proteins and in the retro translocation of misfolded proteins from the endoplasmic reticulum into the cytoplasm.
Why it matters
This review describes inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia, caused by mutations in the VCP gene, with myopathy in about 90% of affected people and premature frontotemporal dementia in a third. It concerns a distinct inherited disorder and does not address treating, curing or preventing Alzheimer's disease.
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Amyloid precursor protein (APP) mis-processing and aberrant tau hyperphosphorylation are causally related to the pathogenesis and neurodegenerative processes that characterize Alzheimer's disease (AD).
Why it matters
In a rat neuronal cell line expressing human tau, glucocorticoids triggered Alzheimer's-like changes including abnormal amyloid precursor protein processing and tau hyperphosphorylation. This is cell-based work on a possible contributing factor and does not test any treatment, cure, or prevention.
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Autopsy studies have shown that about 55% of patients with frontotemporal lobar degeneration (FTLD) and 25% of patients with Alzheimer's disease (AD) harbour TDP-43 immunoreactive pathological changes in their brains.
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Abnormal deposition of alpha-synuclein in neurons and glia is implicated in many neurological diseases, such as Parkinson's disease and Dementia with Lewy bodies.
Why it matters
This laboratory study shows that neurons, astrocytes and microglia can clear extracellular alpha-synuclein aggregates, with microglia degrading them fastest, and that LPS activation slowed degradation. It concerns alpha-synuclein, linked to Parkinson's disease and dementia with Lewy bodies, and reports no Alzheimer's treatment or outcome.
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Temporal lobe epilepsy (TLE) is considered primarily a limbic disorder.
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DNA damage is a form of cell stress and injury that has been implicated in the pathogenesis of many neurologic disorders, including amyotrophic lateral sclerosis, Alzheimer disease, Down syndrome, Parkinson disease, cerebral ischemia, and head trauma.
Why it matters
This review notes that DNA damage has been linked to Alzheimer disease and other neurologic disorders, but that most data show only associations and its role as a direct cause of neuron death remains unclear. It identifies no treatment or prevention for Alzheimer's disease.
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Exercise is a treatment paradigm that can ameliorate cognitive dysfunction in Alzheimer disease (AD) and AD mouse models.
Why it matters
In aged Tg2576 mice with existing Alzheimer's-like pathology, short-term voluntary exercise improved cognition and altered neuroinflammation. Because this was done in mice, it does not establish that exercise produces the same cognitive benefit in people with Alzheimer's disease.
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As the average ages of North Americans and Europeans continue to rise; similarly the incidence of "old age" associated illnesses likewise increases.
Why it matters
Alzheimer's disease, Parkinson's disease and stroke affect different brain regions and cell types early on, but their final stages may share similar cellular and molecular processes leading to neuronal death. The paper discusses TNF-alpha inhibition as a possible treatment strategy, but no trial results in patients are reported here.
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In a previous study, we found that human neural stem cells (HNSCs) exposed to high concentrations of secreted amyloid-precursor protein (sAPP) in vitro differentiated into mainly astrocytes, suggesting that pathological alterations in APP processing during neurodegenerative conditions such as Alzheimer's disease (AD) may prevent neuronal differentiation of HNSCs.
Why it matters
In this mouse study, treatment with (+)-phenserine reduced amyloid precursor protein and GFAP levels in the hippocampus and increased neuronal differentiation of transplanted human neural stem cells. Because it is an animal study, it does not show whether this approach would work in people with 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.
- Brain Functional Magnetic Resonance Imaging Highlights Altered Connections and Functional Networks in Patients With Hypertension
- Brain-derived neurotrophic factor val66met polymorphism and volume of the hippocampal formation
- Genome-wide RNAseq study of the molecular mechanisms underlying microglia activation in response to pathological tau perturbation in the rTg4510 tau transgenic animal model
- Targeting the HDAC2/HNF-4A/miR-101b/AMPK Pathway Rescues Tauopathy and Dendritic Abnormalities in Alzheimer's Disease
- Neuropathological measures of increased tau phosphorylation across the Down syndrome lifespan
- Altered Intrinsic Pyramidal Neuron Properties and Pathway-Specific Synaptic Dysfunction Underlie Aberrant Hippocampal Network Function in a Mouse Model of Tauopathy
- Systematic review and meta-analysis of human transcriptomics reveals neuroinflammation, deficient energy metabolism, and proteostasis failure across neurodegeneration
- Association of GBA Mutations and the E326K Polymorphism With Motor and Cognitive Progression in Parkinson Disease
- Plasma proteins predict conversion to dementia from prodromal disease
- Potential role of Amyloid-β on the association between Orexin-A and blood-brain barrier leakage of globus pallidus in Alzheimer’s disease and dementia with lewy bodies