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Tau pathology, sleep disruption, and hippocampal memory decline in older adults

老年人的 Tau 蛋白病理学、睡眠中断和海马记忆衰退

基本信息

批准号：
9449097
负责人：
Matthew P Walker
金额：
$ 437.88万
依托单位：
UNIVERSITY OF CALIFORNIA BERKELEY
依托单位国家：
美国
项目类别：
财政年份：
2017
资助国家：
美国
起止时间：
2017-09-15 至 2022-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9449097
关键词：
Address Adult Advocate Age Aging Alzheimer&apos s Disease Amyloid Amyloid beta-Protein Behavioral Biological Markers Brain Cerebrospinal Fluid Clinical Cognition Cognitive Consequentialism Data Dementia Detection Deterioration Diagnosis Elderly Electroencephalography Failure Functional Magnetic Resonance Imaging Functional disorder Future Health Health Policy Hippocampus (Brain)Human Impaired cognition Impairment Individual Intervention Link Longevity Measures Medial Memory Memory Loss Memory impairment Pathologic Pathology Pathway interactions Physicians Physiology Positron-Emission Tomography Public Health Risk Rodent Rodent Model Role Severities Sleep Slow-Wave Sleep Symptoms Tauopathies Temporal Lobe Testing Therapeutic Transact age related cognitive development density design follow up assessment follow-up improved in vivo long term memory memory consolidation mild cognitive impairment mouse model new therapeutic target non rapid eye movement novel overexpression protein aggregation restoration sleep abnormalities symptomatology tau Proteins tau aggregation

项目摘要

Project Summary/Abstract: Marked sleep disruption has long been recognized as a prevalent feature of Alzheimer's disease. However, a corpus of new data suggests that sleep abnormalities are not simply a symptom of aging and Alzheimer's disease, but an intimate and bi-directional component of their pathophysiology that further contributes to impairments in long-term memory consolidation. Despite these emerging links, the pathological role of tau protein aggregation in disrupting human NREM sleep physiology remains un-investigated, as does the potential consequence of such disruption for explaining impaired long-term memory consolidation in Alzheimer's disease. Moreover, the longitudinal inter-relationship between tau aggregation, NREM sleep physiology deterioration, and the impairment in hippocampal memory that typifies Alzheimer's disease, is also unknown. Addressing these questions, this proposal will test the hypothesis that early accumulation of tau in the human medial temporal lobe selectively impairs NREM sleep oscillations, thereby diminishing long-term memory consolidation and associated aspect of cognition, both cross-sectionally and longitudinally. Such findings may help identify a unique mechanistic pathway (sleep disruption) through which Alzheimer's disease pathology transacts memory impairment, and further define a new therapeutic target (sleep restoration) for intervention in aging and Alzheimer's disease. Additionally, such data would motivate a greater sensitivity of physicians to inquire about, diagnose and treat sleep difficulties across all ages. More generally, support for our hypothesis would argue for improved public health policies advocating for sufficient quality sleep throughout adulthood—a memorandum that may lower dementia risk and maintain cognitive health across the populous.

项目摘要/摘要：明显的睡眠障碍长期以来被认为是睡眠障碍的普遍特征