Top Research Papers on Alzheimer's Disease

Lecanemab reduced markers of amyloid in early Alzheimer's disease and resulted in moderately less decline on measures of cognition and function than placebo at 18 months but was associated with adverse events.

This article describes the public health impact of Alzheimer's disease, including prevalence and incidence, mortality and morbidity, use and costs of care, and the overall impact on family caregivers, the dementia workforce and society. The Special Report examines the patient journey from awareness of cognitive changes to potential treatment with drugs that change the underlying biology of Alzheimer's. An estimated 6.7 million Americans age 65 and older are living with Alzheimer's dementia today. This number could grow to 13.8 million by 2060 barring the development of medical breakthroughs to...

An integrated biological and clinical staging scheme is described that accommodates the fact that common copathologies, cognitive reserve, and resistance may modify relationships between clinical and biological AD stages.

This article describes the public health impact of Alzheimer's disease (AD), including prevalence and incidence, mortality and morbidity, use and costs of care and the ramifications of AD for family caregivers, the dementia workforce and society. The Special Report discusses the larger health care system for older adults with cognitive issues, focusing on the role of caregivers and non‐physician health care professionals. An estimated 6.9 million Americans age 65 and older are living with Alzheimer's dementia today. This number could grow to 13.8 million by 2060, barring the development of med...

The most consistent findings were for Zn and Cu, with most studies observing a decrease in Zn levels and an increase in Cu levels in AD patients, but several studies found no such relation.

Heterogeneity of Alzheimer's disease predicts complex clinical presentations in people living with AD and may raise awareness of a healthy lifestyle as potential prevention and treatment of the comorbidities.

Patients and families need hope, not false hope

Alzheimer's disease (AD) is the most common type of dementia, accounting for 60% to 80% of all cases [...].

Some current ideas on processes in inflammaging that appear to drive the neurodegenerative process in AD are discussed and a few immunomodulatory strategies being developed to selectively target the detrimental aspects of neuroinflammation without affecting defense mechanisms against pathogens and tissue damage are summarized.

Findings from human and non-human studies examining the association of metformin with AD/ADRD related outcomes suggest that met formin use in persons with T2D is associated with a lower risk of dementia.

It is imperative to comprehend the intricate mechanisms that result in microglial impairment to develop new immunomodulating therapies that primarily attempt to recover the physiological role of microglia, allowing them to carry out their core function of brain protection.

The impact of the most common comorbidities in the clinical management of AD patients are discussed and drugs commonly prescribed to patients with diabetes and cardiovascular disease have shown promising results.

The data from the phase 3 clinical trials in mildly symptomatic individuals with AD demonstrate that Aβ reduction has modest clinical benefit, which supports the central tenet of the amyloid cascade hypothesis (ACH), which proposes that Aβ deposits play a causal, initiating role in AD.

New trial reports little to celebrate for patients and carers, and calls for more to be done to support people with mental health needs.

The role of the inflammatory processes in developing neurodegeneration, activated during physiological aging and due to various diseases such as atherosclerosis, obesity, type 2 diabetes mellitus, and depressive disorders are discussed.

In patients with early symptomatic Alzheimer's disease, donanemab resulted in a better composite score for cognition and for the ability to perform activities of daily living than placebo at 76 weeks, although results for secondary outcomes were mixed.

A brief overview of the current knowledge regarding the role of epigenetics (including mitoepigenetics) in AD is provided, and the possibility of applying these advances for future AD therapy is provided.

This MR study supports a causal link between AD, amyloid pathology, and generalized epilepsy and indicates a close association between AD and focal HS.

The public health impact of Alzheimer's disease (AD), including incidence and prevalence, mortality and morbidity, use and costs of care, and the overall impact on family caregivers, the dementia workforce and society are described are described.

Improved developments in fluid and imaging biomarkers have led to the improved understanding of AD as a chronic condition with a protracted presymptomatic phase followed by the clinical stage traditionally recognized by neurologists.

New small-molecule modulators of the Hedgehog signalling pathway are identified, which is known to drive tumorigenesis and GPR39 is a new component in Hedgehog signalling, and the inhibitors will be useful to study this receptor.

Various epigenetic changes in AD are summarized, including DNA methylation, histone modification and miRNA, and it is concluded that epigenetics has great potential as a new target for the treatment of AD.

The authors can slow Alzheimer’s but cannot prevent or stop it till now, so some non-drug treatments, like physical activity, social engagement, nutritious supplemented food, and FDA approved drugs helps to reduce AD.

There are many different mechanisms by which excess levels of propionate may lead to AD, such as hyperammonemia, and these mechanisms offer potential points for intervention.

Mechanisms by which excess ECM accumulation may contribute to AD pathology are described and pathological ECM alterations that occur in AD as well as conditions that increase the AD risk.

This review addresses the multiple ways in which abnormal mitochondrial structure and function contribute to AD, and suggests that restoring mitochondrial health may be a viable approach to AD treatment.

The heterogeneity of Alzheimer’s disease predicts complex clinical presentations in people living with AD, and the genes define AD as a part of age-related comorbidities with shared biological mechanisms and may raise awareness of a healthy lifestyle as potential prevention and treatment of the comorbidities.

This review highlighted the main histone modifications and their functional role, including histone acetylation, histone methylation, and histone phosphorylation, as well as changes in such hist one modifications that occur in the aging process and mainly in Alzheimer’s disease (AD).

Evidence from clinical, imaging, neuropathological, and animal studies supporting vascular contributions to the onset and progression of AD pathology support the notion that the onset of AD may be primarily influenced by vascular, rather than neurodegenerative, mechanisms.

The public health impact of Alzheimer's disease (AD), including incidence and prevalence, mortality and morbidity, use and costs of care, and the overall impact on caregivers and society is described, is described.

Tests using a lumbar puncture or PET scan can help to confirm the diagnosis of Alzheimer's disease, but they are only used in special circumstances and you can reduce your risk of developing Alzheimer’s disease by eating a Mediterranean-style diet, engaging in aerobic exercise, and staying socially active.

Although substantial progress has been made in the last two decades, there are still important unfilled gaps in the understanding of the pathomechanism of Alzheimer's disease (AD) [...].

The Alzheimer’s Disease Variant Portal (ADVP) is a valuable resource for investigators to quickly and systematically explore high-confidence AD genetic findings and provides insights into population-specific AD genetic architecture.

A mini review explores fall risk factors in symptomatic AD, evidence for effective fall prevention interventions in symptomatic AD, and preclinical AD as an avenue for future falls research, including recommendations for future research directions to improve the understanding of falls and fall risk during preclinical AD.

There is robust evidence for the use of acetylcholinesterase inhibitors for patients with mild, moderate, and severe dementia due to AD, including outcomes beyond changes in cognitive screening test scores, and limited studies support the use of memantine in moderate and severe stages.

The current understanding of Alzheimer disease, including the natural history, common risk factors, and expected progression of AD neuropathologic change are reviewed so that neurologists can apply this knowledge to identify patients with symptoms, signs, and findings on common diagnostic tests consistent with AD.

The role of immune responses in AD is discussed, focusing on the contribution of T‐cells, which play a pivotal role in immunity in the central nervous system during disease initiation and exacerbation.

This review focuses on the autophagy function in microglia and its dysfunction in AD andPD disease models in an attempt to help the understanding of the pathogenesis and identifying new therapeutic targets of AD and PD.

Additional data are needed before use of BBMs as stand‐alone diagnostic AD markers, or before considering use in primary care, and it is recommended to cautiously start using BBMs in specialized memory clinics as part of the diagnostic work‐up of patients with cognitive symptoms.

This review will summarize the advantages and limitations of various mouse models of AD, including transgenic, knock-in, and injection models based on Aβ and tau, and other mouse modelsBased on neuroinflammation because recent genetic studies have suggested that microglia are crucial in the pathogenesis of AD.

The widely accepted view of one, dimorphic disease through the prism of the Bmi1+/– mouse model and the distinct chromatin signatures observed between SLOAD and FEOAD brains are interrogated.

Solanezumab, which targets monomeric amyloids in persons with elevated brain amyloid levels, did not slow cognitive decline as compared with placebo over a period of 240 weeks in people with preclinical Alzheimer's disease.

The current knowledge about the state of AHN in AD patients, AHN impairment as a potentially relevant mechanism underlying memory deficits in AD, therapeutic potential of activating AHNin AD, and the mechanisms ofAHN impairment in AD are outlined and discussed.

The mere presence of infectious agents is suspected to induce both local and systemic inflammatory responses promoting cellular damage and neuronal loss within the context of AD.

The current literature on racial disparities in AD and ADRD is examined, particularly concerning AA caregivers, with growing recognition that AD andADRD pose a significant stress on AA caregivers compared to white people.

Writing disorders are multi-componential in AD and not strictly limited to one processing level, and the slow and poorly automated execution of motor programs is not bound to alphabetical material.

The influence of registration and brain extraction on the learned features by heat mapping was investigated and a novel relevance-guided training method was compared, focusing on brain tissue, yielded highest classification accuracies and confirmed histopathologically relevant regional iron deposition.

The role of cholinergic signaling and the correlation between the cholinerential signaling pathway with other risk factors in AD is summarized and the latest research about the efficient therapeutic drugs and treatment of AD is provided.

OBJECTIVE This article provides a comprehensive review of the distinct features of four atypical Alzheimer disease (AD) variants: dysexecutive AD, behavioral variant AD, posterior cortical atrophy, and the logopenic variant of primary progressive aphasia. It also elucidates their clinical presentations, underlying pathophysiologic pathways, diagnostic indicators, and management requirements. LATEST DEVELOPMENTS Recent research has revealed that these atypical AD forms vary not only in clinical manifestations but in their functional neuroanatomy spanning a common pathophysiologic spectrum. Im...

The properties of the key proteins comprising the amyloid plaques and neurofibrillary tangles that define the neuropathology of AD have been identified and combined with extensive genetic studies, a sequence of lesion formation in brain networks serving memory and cognition is suggested.