Principal component analysis suggests multiple dimensions of memory inhibition that are differentially affected by age.

Background: Cognitive inhibition is among the executive functions that decline early in the course of normal aging. Failures to be able to inhibit irrelevant information from memory may represent an essential factor of age-associated memory impairment. While a variety of elaborate behavioral tasks have been developed that presumably all index memory inhibition, the extent to which these different tasks measure the same underlying cognitive construct that declines with age has not been well explored.

Effects of white matter hyperintensities distribution and clustering on late-life cognitive impairment.

White matter hyperintensities (WMH) are a key hallmark of subclinical cerebrovascular disease and are known to impair cognition. Here, we parcellated WMH using a novel system that segments WMH based on both lobar regions and distance from the ventricles, dividing the brain into a coordinate system composed of 36 distinct parcels ('bullseye' parcellation), and then investigated the effect of distribution on cognition using two different analytic approaches. Data from a well characterized sample of healthy older adults (58 to 84 years) who were free of dementia were included.

Association Between Cognitive Test Performance and Subjective Cognitive Decline in a Diverse Cohort of Older Adults: Findings From the KHANDLE Study.

Background: Subjective cognitive decline (SCD) may represent a low-burden indicator of dementia risk. The value of SCD as a proxy marker, however, depends on the consistency of associations between subjective and objective cognitive measures across sociodemographic and psychological factors.

Methods: We evaluated baseline data from the Kaiser Healthy Aging and Diverse Life Experiences (KHANDLE) study (n=1615).

Protein interacting with Amyloid Precursor Protein tail-1 (PAT1) is involved in early endocytosis.

Protein interacting with Amyloid Precursor Protein (APP) tail 1 (PAT1) also called APPBP2 or Ara 67 has different targets such as APP or androgen receptor and is expressed in several tissues. PAT1 is known to be involved in the subcellular trafficking of its targets. We previously observed in primary neurons that PAT1 is poorly associated with APP at the cell surface.

Distinct dynamic profiles of microglial activation are associated with progression of Alzheimer's disease.

Although brain neuroinflammation may play an instrumental role in the pathophysiology of Alzheimer's disease, its actual impact on disease progression remains controversial, being reported as either detrimental or protective. This work aimed at investigating the temporal relationship between microglial activation and clinical progression of Alzheimer's disease. First, in a large cohort of patients with Alzheimer's disease we analysed the predictive value of microglial activation assessed by 18F-DPA-714 PET imaging on functional, cognitive and MRI biomarkers outcomes after a 2-year follow-up.

Systemic inflammation as a predictor of brain aging: Contributions of physical activity, metabolic risk, and genetic risk.

Inflammatory processes may contribute to risk for Alzheimer's disease (AD) and age-related brain degeneration. Metabolic and genetic risk factors, and physical activity may, in turn, influence these inflammatory processes. Some of these risk factors are modifiable, and interact with each other.

Increasing membrane cholesterol of neurons in culture recapitulates Alzheimer's disease early phenotypes.

Background: It is suspected that excess of brain cholesterol plays a role in Alzheimer's disease (AD). Membrane-associated cholesterol was shown to be increased in the brain of individuals with sporadic AD and to correlate with the severity of the disease. We hypothesized that an increase of membrane cholesterol could trigger sporadic AD early phenotypes.

Two distinct amnesic profiles in behavioral variant frontotemporal dementia.

Background: Whether or not episodic memory deficit is a characteristic of behavioral variant frontotemporal dementia (bvFTD) is a crucial question for its diagnosis and management.

Methods: We compared the episodic memory performance profile of bvFTD patients with healthy control subjects and patients with Alzheimer's disease (AD) as defined by clinical and biological criteria. Episodic memory was assessed with the Free and Cued Selective Reminding Test, which controls for effective encoding and identifies memory storage ability resulting from consolidation processing.

Distinct patterns of antiamyloid-β antibodies in typical and atypical Alzheimer disease.

Objective: To compare serum antiamyloid-β (Aβ) antibodies in typical and atypical Alzheimer disease (AD).

Design: Preliminary observations.

Subjects: Thirteen patients with AD, 8 patients with posterior cortical atrophy with evidence of AD (PCA-AD) pathophysiological process by both cerebrospinal fluid (CSF) biomarkers and amyloid imaging, and 12 age-matched control individuals.

Brain networks in posterior cortical atrophy: a single case tractography study and literature review.

Posterior cortical atrophy (PCA) is rare neurodegenerative dementia, clinically characterized by a progressive decline in higher-visual object and space processing. After a brief review of the literature on the neuroimaging in PCA, here we present a study of the brain structural connectivity in a patient with PCA and progressive isolated visual and visuo-motor signs. Clinical and cognitive data were acquired in a 58-years-old patient (woman, right-handed, disease duration 18 months).

Similar amyloid-β burden in posterior cortical atrophy and Alzheimer's disease.

While the clinical presentation of posterior cortical atrophy is clearly distinct from typical Alzheimer's disease, neuropathological studies have suggested that most patients with posterior cortical atrophy have Alzheimer's disease with an atypical visual presentation. We analysed in vivo pathophysiological markers of Alzheimer's disease such as cerebrospinal fluid biomarkers and positron emission tomography imaging with ¹¹C-labelled Pittsburgh compound-B in posterior cortical atrophy to determine whether biochemical profile and fibrillar amyloid-β burden topography are associated with the clinical presentation. Nine patients with posterior cortical atrophy and nine with typical Alzheimer's disease individually matched for age, duration and severity of the disease and 10 cognitively normal age-matched controls were included.