https://hms.harvard.edu/news/sporadic-alzheimers-dish
A new model of sporadic Alzheimer's disease, which accounts for more than 90 percent of cases, reveals molecular abnormalities in neural stem cells. The study suggests that REST, a protein that protects against age-related cognitive decline, is disrupted in Alzheimer's cells and may be a drug target.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9966419/
Alzheimer's disease (AD) is the most common neurodegenerative disease in the world. It is classified as familial and sporadic. The dominant familial or autosomal presentation represents 1-5% of the total number of cases. It is categorized as early onset (EOAD; <65 years of age) and presents genetic mutations in presenilin 1 ( PSEN1

https://pubmed.ncbi.nlm.nih.gov/24852227/
The increasing prevalence of Alzheimer's disease (AD) and a lack of effective prevention or disease-modifying therapies are global challenges with devastating personal, social and economic consequences. The amyloid β (Aβ) hypothesis posits that cerebral β-amyloidosis is a critical early event in AD pathogenesis.

https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/symptoms-causes/syc-20350447
Alzheimer's disease is the most common cause of dementia — a gradual decline in memory, thinking, behavior and social skills. These changes affect a person's ability to function. ... Swaddiwudhipong N, et al. Pre-diagnostic cognitive and functional impairment in multiple sporadic neurodegenerative diseases. Alzheimer's and Dementia. 2022; doi

https://www.alz.org/help-support/i-have-alz/younger-onset
Alzheimer's disease is considered to be younger-onset Alzheimer's if it affects a person under 65. Younger-onset can also be referred to as early onset Alzheimer's. People with younger-onset Alzheimer's can be in the early, middle or late stage of the disease. The majority of people with younger-onset have sporadic Alzheimer's disease

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8509365/
1. Introduction and Background. This review aims to highlight the similarities and differences between the clinical and neuropathological manifestations of Alzheimer's disease (AD) in sporadic (or late-onset AD) and autosomal dominant AD (ADAD) and Down syndrome-associated AD (DSAD).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7421532/
Discussion. The trajectory in sporadic AD is led by Aβ accumulation, followed by CSF t‐tau increase, memory deficits, brain atrophy, hypometabolism, and cognitive decline. Keywords: amyloid beta, Alzheimer's disease, biomarkers, clinical, tau. Go to: 1. BACKGROUND. Alzheimer's disease (AD) is a neurodegenerative disorder clinically

https://theconversation.com/what-causes-alzheimers-disease-what-we-know-dont-know-and-suspect-75847
The strongest genetic risk factor for sporadic Alzheimer's disease is a gene called " apolipoprotein E (APOE) ε4 ", and emerging research suggests this increased risk may be due to

https://www.nature.com/articles/nrdp201556
Sporadic Alzheimer's disease is the most common type and has a mean age of onset of 80 years. The main cause is the failure to clear Aβ peptide from the brain tissue. However, co-morbidities such

https://www.nature.com/articles/s41380-018-0255-6
Integrative gene network approaches enable new avenues of exploration that implicate causal genes in sporadic late-onset Alzheimer's disease (LOAD) pathogenesis, thereby offering novel insights

https://www.nature.com/articles/s41583-021-00533-w
We propose three Alzheimer disease (AD) variants — autosomal dominant AD, APOE ε4-related sporadic AD and APOE ε4-unrelated sporadic AD — on the basis of genetic backgrounds and featuring

https://medicine.iu.edu/news/2022/01/New-study-shows-pathological-differences-in-inherited-versus-sporadic-Alzheimers-disease
Patients had either sporadic Alzheimer's disease or dominantly inherited Alzheimer's disease with a mutation in the APP or PSEN1 genes. "This new knowledge of the filament structures provides deeper insights into the disease process in Alzheimer's and may lead to the development of compounds that can prevent the disease by inhibiting

https://alzheimersprevention.org/alzheimers-info/risk-factors/
Alzheimer's disease, on the other hand, is not caused by a single gene. The two basic types of Alzheimer's are Familial and Sporadic: Familial - Familial Alzheimer's disease (FAD) is a rare form of early-onset Alzheimer's, affecting less than 10 percent of Alzheimer's patients.

https://pubmed.ncbi.nlm.nih.gov/23276979/
Alzheimer's disease (AD) is an age-related progressive neurodegenerative disorder. A majority of cases manifest as a late onset sporadic form but genetically the disease is divided into familial cases and sporadic cases. The familial form is due to mutations in three major genes (amyloid precursor protein (APP) gene, presenilin1 (PSEN1) gene

https://onlinelibrary.wiley.com/doi/10.1002/advs.202101462
1 Introduction. Alzheimer's disease (AD) is a progressive neurodegenerative disease with no cure, characterized by extracellular amyloid beta (Aβ) plaques, intracellular phosphorylated microtubule-associated tau protein (p-Tau) tangles, and age-related memory loss.Over 50 million people worldwide are believed to live with AD or other dementia, and 5.8 million Americans suffer from AD in 2019. []

https://alz-journals.onlinelibrary.wiley.com/doi/toc/10.1002/(ISSN)1552-5279.research-advances-EOAD
The Alzheimer's Association is the largest non-profit funder of Alzheimer's disease research. Its mission is "to eliminate Alzheimer's disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health". ISTAART; AAIC Conference

https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.12032
1 BACKGROUND. Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) deposition, tau pathology, neurodegeneration, and cognitive decline. 1 Diagnosing and staging AD has been greatly facilitated by in vivo biomarkers including positron-emission tomography (PET) and cerebrospinal fluid (CSF) markers of Aβ and pathologic tau, as well as volumetric magnetic resonance imaging (MRI) and

https://www.medicalnewstoday.com/articles/early-stage-research-suggests-new-way-to-fight-alzheimers-disease-progression
About 32 million people globally have Alzheimer's disease. Researchers continue to look for a way to stop or slow disease progression. Researchers from the Icahn School of Medicine at Mount

https://www.tandfonline.com/doi/full/10.1586/14737175.2014.915740
The increasing prevalence of Alzheimer's disease (AD) and a lack of effective prevention or disease-modifying therapies are global challenges with devastating personal, social and economic consequences. The amyloid β (Aβ) hypothesis posits that cerebral β-amyloidosis is a critical early event in AD pathogenesis.

https://pubmed.ncbi.nlm.nih.gov/26971934/
Alzheimer's disease (AD) is a multifactorial disease with genetic (70%) and environmental (30%) causes. Among the genetic factors are genes associated with a family history of the disease (familial AD, FAD) and sporadic AD (SAD). The genes: APP (amyloid precursor protein), PSEN1 (Presenilin 1) and PSEN2 (Presenilin 2) are responsible for the

https://www.nature.com/articles/s41582-024-00940-4
However, the term 'Alzheimer disease' misrepresents the sporadic, late-onset form of the condition, as it deviates from the case described by Alois Alzheimer in 1907 (ref. 73), which involved

https://www.pnas.org/doi/10.1073/pnas.1201632109
Alzheimer's disease (AD) is the most common form of dementia, with a predicted incidence in the global population of 1 in 85 by 2050 ().The disease is degenerative, eventually leading to death, and there is currently no cure; therefore insights into the molecular causes of the disease are urgently required (2, 3).AD is pathologically characterized by the presence of amyloid plaques and

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4509477/
The growing literature of metabolic risk factors of sporadic Alzheimer's disease (AD) extending from epidemiology to molecular pathogenesis and therapeutic management, however, is replete with controversies and contradictions. Nevertheless, this is an active area of research and one that holds enormous promise in the future development of

https://health.usnews.com/senior-care/articles/stages-of-alzheimers
Eating a plant-rich diet that is mindful of excess carbohydrates and focused on fiber and probiotics. Exercising with a combination of aerobics and strength training. Sleeping seven to eight hours

https://www.everydayhealth.com/alzheimers-disease/lifestyle-changes-may-reverse-early-alzheimers-symptoms/
The study randomly assigned 51 people in the early stages of Alzheimer's disease to either stick to their usual routines for 20 weeks or make intensive changes to adopt four new habits:

https://medicalxpress.com/news/2024-06-alzheimer-reversed-documentary.html
Alzheimer's disease can be split in two subgroups, familial and sporadic. Only 5% of patients with Alzheimer's are familial , inherited, and 95% of Alzheimer's patients are sporadic , due to

https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/dad2.12095
1 BACKGROUND. Alzheimer's disease (AD) is a neurodegenerative disorder clinically characterized by early memory loss and progressing into dementia. 1 It has been documented that amyloid beta (Aβ) deposition, tau pathology, and neuronal degeneration precede clinical symptoms. 2-6 The long preclinical phase of AD is an opportunity to identify the changes in pathophysiological biomarkers that

https://www.science.org/doi/10.1126/science.add6260
Alzheimer's disease (AD) makes up 60 to 80% of all dementia cases and is one of the top 10 causes of death, with no effective prevention or treatment available. AD is a neurodegenerative disease, pathologically defined by the progressive buildup in the brain of two types of proteinaceous deposits, amyloid β (Αβ) and tau tangles.

https://www.cell.com/cms/10.1016/j.neuron.2024.02.009/attachment/b2e4957f-6bfe-4308-a564-bfcdde17af36/mmc1.pdf
an autosomal dominant Alzheimer's disease profile and possible mechanisms of disease protection Maria Camila Almeida, Sarah J. Eger, Caroline He, Morgane Audouard, Arina ... in nuclei from sporadic AD (p = 0.03) compared to controls. (E) Heatmap showing the z-score for the levels of expression of the upregulated and

https://pubmed.ncbi.nlm.nih.gov/37744023/
Abstract. Genome-wide association studies have identified multiple Alzheimer's disease risk loci with small effect sizes. Polygenic risk scores, which aggregate these variants, are associated with grey matter structural changes. However, genome-wide scores do not allow mechanistic interpretations. The present study explored associations between