When discussing the concept of cognitive impairment, many terms are used, including dementia, amnestic disorder, cognitive impairment not dementia (CIND), cognitive impairment associated with normal aging, mild cognitive impairment, vascular cognitive impairment,… Read More
Nonamnestic mild cognitive impairment, a putative precursor of vascular and other non-Alzheimer dementias, is hypothesized to have a vascular etiology. ... Setting? Olmsted County, Minnesota. Participants? A total of 2719 participants were evaluated at
Cognitive impairment and dementia are common after stroke. It is unclear if risk differs between ischaemic stroke subtypes. Lacunar strokes might be less likely to affect cognition than more severe, larger cortical strokes, except that lacunar strokes are associated with cerebral small vessel disease (SVD), which is the commonest vascular cause of dementia.
We searched MEDLINE and PsychINFO for studies of mild cognitive impairment (MCI) or dement
We also used subcategories of MCI ( amnestic and nonamnestic), and dementia ( probable Alzheimer disease and vasculardementia, including possible Alzheimer disease with stroke). ... Persons with MCI and coexisting depression at baseline had a higher
Question: How effective and safe are cholinesterase inhibitors for mild cognitive impairment?
Outcomes: Progression to dementia or Alzheimer's disease (National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's disease and Related Disorders Association (NINDS-ARDRA), International Classification of Diseases (ICD)-10 or Diagnostic and Statistical Manual (DSM-IV criteria), dementia with Lewy bodies or vasculardementia (
Parental stroke has been related to an increased risk of stroke in the offspring. This study examines whether parental stroke is also associated with increased vascular brain injury and poorer cognitive performance among offspring free of clinical stroke.
Multivariable regression analyses were used to relate parental stroke to cross-sectional and change in brain magnetic resonance imaging measures and cognitive func
Life expectancy is rising however with more people living longer there is a concomitant rise in the incidence of dementia. In addition to age-related cognitive decline there is a higher risk of going on to develop vasculardementia and Alzheimer's disease associated with aspects of modern lifestyle. Most worryingly, recent data reports accelerated cognitive decline in adolescents associated with poor diet (high fat and calorie intake). Thus the increase in dementia in 'old-age' may have as much to do with 'new-age' lifestyle as it does with normal ageing. It would seem wise therefore to investigate the molecular connections between lifestyle and cognitive decline in more detail. Epidemiological evidence suggests an increased risk of developing dementia (including Alzheimer's disease) in individuals with obesity and type 2 diabetes but also in those with poor insulin sensitivity without diabetes, implicating a mechanistic link between adiposity, insulin sensitivity and dementia.
Bilateral temporal lobe hyperintensity (BTH) is a commonly encountered MRI finding in a wide spectrum of clinical conditions and often poses a diagnostic challenge to the radiologist. The purpose of this paper is to elucidate several diseases that manifest as BTH on MRI, based on a retrospective review of cranial MRI of 65 cases seen in our institution between October 2007 and September 2010. We found BTH in different clinical scenarios that included infective diseases (herpes simplex virus, congenital cytomegalovirus infection), epileptic syndrome (mesial temporal sclerosis), neurodegenerative disorders (Alzheimer's disease, frontotemporal dementia, Type 1 myotonic dystrophy), neoplastic conditions (gliomatosis cerebri), metabolic disorders (mitochondrial encephalopathy, lactic acidosis and stroke-like episodes, Wilson's disease, hyperammonemia), dysmyelinating disease (megalencephalic leukoencephalopathy with subcortical cysts), and vascular (cerebral autosomal dominant arteriopathy
VaD is the second-most common form of dementia, second only to that caused by AD. As the name indicates, VaD is predominantly considered a disease caused by vascular phenomena.|In this invited review, we introduce the reader to recent developments in defining VaD as a unique form of dementia by reviewing the current pertinent literature. We discuss the clinical and experimental evidence that supports the notion that the microcirculation, specifically cell-to-cell communication, likely contributes to the development of VaD. Through exploration of the concept of the NVU, we elucidate the extensive cerebrovascular communication that exists and highlight models that may help test the contribution(s) of cell-to-cell communication at the microvascular level to the development and progression of VaD. Lastly, we explore the possibility that some dementia, generally considered to be purely neurodegenerative, may actually have a vascular component at the neurovascular level.|This latter
Dementia has become a relevant problem associated with the elderly in our countries. Increased interest in the field has yielded a copious literature, so far mostly centered on Alzheimer's dementia. Cerebrospinal fluid (CSF) analysis combined with neuropsychology, even in absence of neuroimaging, represents the gold standard to reach a diagnosis when cortical cognitive impairment prevails. In view of this, low levels of CSF amyloid peptides (A) and high tau/A protein ratio, despite prominent impairment of executive functions or concomitant vascular burden, facilitate the diagnosis of Alzheimer's disease. Conversely, an early cognitive impairment occurring in patients suffering from Parkinson's disease (PD) or Lewy body disorders (LBDs), both diagnoses posed on pure clinical grounds, remains quite elusive in term of biomarkers or neuropsychological assessment. Whether PD with dementia (PDD) and dementia with Lewy bodies (DLB) represent further steps along with a continuum of the
As the population ages, the economic and societal impacts of neurodegenerative and neuropsychiatric disorders are expected to rise sharply. Like dementia, late-life depressive disorders are common and are linked to increased disability, high healthcare utilisation, cognitive decline and premature mortality. Considerable heterogeneity in the clinical presentation of major depression across the life cycle may reflect unique pathophysiological pathways to illness; differentiating those with earlier onset who have grown older (early-onset depression), from those with illness onset after the age of 50 or 60 years (late-onset depression). The last two decades have witnessed significant advances in our understanding of the neurobiology of early- and late-onset depression, and has shown that disturbances of fronto-subcortical functioning are implicated. New biomedical models extend well beyond perturbations of traditional monoamine systems to include altered neurotrophins, endocrinologic and