Clinical Manifestations.

Background: Neurocognitive health is influenced by multiple modifiable and non-modifiable lifestyle factors. Machine learning tools offer a promising approach to better understand complex models of cognitive function. We used extreme gradient boosting (XG Boost), an algorithm of decision-tree modeling, to analyze the association between 15 late-life lifestyle and demographic factors with episodic memory performance.

Clinical Manifestations.

Background: Few studies have investigated the relationship between subjective cognitive concerns and objective cognitive decline in the oldest-old or examined gender differences. We evaluated this association and stratification by gender in a diverse cohort of adults ages 90+.

Methods: LifeAfter90 is an ongoing cohort of adults ages 90+.

Clinical Manifestations.

Background: Depressive symptoms are associated with reduced brain integrity. However, it is unclear if this association holds among a racially and ethnically diverse population aged ≥90 years and if there are differences by gender.

Method: The LifeAfter90 Study enrolled 212 long-term members of Kaiser Permanente Northern California who were ≥90 years old, without dementia diagnosis, and received neuroimaging via 3T MRI.

Overcoming boundary conditions for object location memory destabilization in male rats involves dopamine D1 receptor activation.

Consolidated long-term memories can undergo strength or content modification via protein synthesis-dependent reconsolidation. This is the process by which a reminder cue initiates reactivation of the memory trace, triggering destabilization. Older and more strongly encoded spatial memories can resist destabilization due to biological boundary conditions.

The impact of sphingomyelin on the pathophysiology and treatment response to olipudase alfa in acid sphingomyelinase deficiency.

Acid sphingomyelinase deficiency (ASMD) is a rare progressive genetic disorder caused by pathogenic variants in the gene causing low or absent activity of the enzyme acid sphingomyelinase, resulting in subsequent accumulation of its substrate, sphingomyelin. Signs and symptoms of excessive lysosomal sphingomyelin storage, such as hepatosplenomegaly and pulmonary impairment, and in a subset of patients, progressive neurological manifestations, have long been recognized as hallmarks of the disease. Uncontrolled accumulation of sphingomyelin has important and complex downstream metabolic and immunologic consequences that contribute to the disease burden.