Top Research Papers on Alzheimer's Disease

There exists evidence suggesting that memory impairment in AD begins with changes in hippocampal synaptic functions and then gradually progresses to neurodegeneration and neuronal loss in patients of AD, and the Aβ-induced damage in hippocampus might underlie some of the AD behavioral deficits.

Memory tests that specifically probe mesiotemporal function in elderly individuals with memory deficits are used, demonstrating that these tests predict CSF Aβ42/tau levels and establishing a neuroanatomic localization for the patient's complaint.

It is suggested that 8-amyloid is translocated to vessel walls via putative ISF drainage pathways and thus accumulates predominantly in the adventitia and outer media of inmcortical and leptomeningeal arteries in CAA.

In their article, “Imaging markers for Alzheimer disease: Which vs how,” Dr. Frisoni and his colleagues looked carefully at the ways in which doctors evaluate Alzheimer disease and another problem with cognition called mild cognitive impairment.

Improved understanding of the clinical onset, progression, neuroimaging, pathologic features, genetics, and other risk factors for AD impacts the approaches to clinical diagnosis and future therapeutic interventions.

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.

The authors' idea was that patients with healthy brains might be able to lose some brain function but have enough reserve that these changes did not result in dementia, but that there might be some important reasons why some patients did not get AD.

Evidence for the prion-like properties of both Aβ and tau individually are discussed, as well as the intriguing possibility that misfolded Aβ acts as a template for tau misfolding in vivo.

It is argued that Alzheimer disease pathology represents a final common pattern of changes that results from several or possibly many different aetiologies, which might better guide future research into late onset dementias.

Dementia, in this context, is re-defined as the differential manifestation of deteriorating brain functions over time as a part of aging due to cell deaths in the brain caused by any neurodegenerative disease.

The symptoms and risk factors for Alzheimer's disease are outlined, and what treatments are currently available are described.

Trusted information on what alzheimer's disease is including signs and symptoms, treatment, who is affected, prevention, and links to trusted resources is provided.

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.

The challenge for the near future will be the development of new therapies and therapeutic targets for disease modification and prevention of Alzheimer's disease.

Techniques providing earlier diagnosis, such as cerebrospinal fluid biomarkers and amyloid positron emission tomography neuroimaging, are key to testing this theory in clinical trials and results from trials of agents such as aducanumab are encouraging but must also be interpreted with caution.

Caregivers play a large role in managing the patient and should be encouraged to seek out adult day care centers, home health services, respite care, and additional social support.

The Hospital of Golitsyn from the first years of its existence has proved to be an advanced medical institution and this is in large part due to Professor EO Mukhin, the remarkable scientist and the doctor-expert, the author of the first national manual on traumatology and orthopaedics, proved himself to be the greatest surgeon of his time.

Advances in understanding the pathogenetic cascade of events that characterize AD provide a framework for early detection and therapeutic interventions, including transmitter replacement therapies, antioxidants, anti-inflammatory agents, estrogens, nerve growth factor, and drugs that prevent amyloid formation in the brain.

It is perhaps premature to rule out circulatory factors, especially since the authors now know about the importance of the extracranial circulation, but arteriosclerotic stenoses could cause cerebrovascular insufficiency which would explain this woman’s fluctuating and progressive symptoms.

Current Alzheimer's disease medications may temporarily improve symptoms or slow the rate of decline, and medications that are approved for symptomatic relief in the U.S.A include Donepezil (Aricept), Rivastigmine (Exelon) and Tacrine (Cognex).