Alzheimer Disease
Conditions
Brief summary
The investigators will evaluate the theory that Alzheimer's disease-related memory impairment derives from the inefficient orchestration of rhythmic activity at the level of large-scale cortical networks. The results as expected to elucidate AD-related pathophysiology and set groundwork for the development of drug-free interventions for improving memory in AD and related dementias.
Detailed description
The investigators hypothesize that AD-related memory impairments emerge from large-scale functional dysconnectivity, and by stimulating the brain noninvasively with extremely weak levels of electrical current, the investigators may be able to re-synchronize connectivity and stabilize or improve memory and cognitive function, measured behaviorally. The experimental intervention involves the application of low-intensity, high-definition, transcranial electrical current stimulation while subjects perform a variety of computer-based tasks that probe memory and cognitive function.
Interventions
Low-intensity and safe, noninvasive application of electrical current to the human scalp with the goal of gradually modulating levels of neuronal excitability.
Sponsors
Boston University Charles River Campus
Study design
Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
BASIC_SCIENCE
Masking
DOUBLE (Subject, Outcomes Assessor)
Eligibility
Sex/Gender
ALL
Age
50 Years to 100 Years
Healthy volunteers
Yes
Inclusion criteria
All subjects. Age 50-100 years. We will equally recruit subjects with respect to gender, race, ethnicity, socioeconomic and other factors to allow the results of this research to yield the greatest generalizability. Mild AD dementia. Meets probable AD dementia NIA-AA criteria 86; MoCA 10-25 85; performance on Uniform Data Set version 3 (UDS-3) delayed recall (Craft Story 21) and recognition (Benson Complex Figure) memory worse than 1.5 SD for age and education; worse than 1.5 SD for age and education in at least one other cognitive domain (e.g., language, executive functioning) based on other tests in the UDS-3. A summary of the NIA-AA criteria for AD dementia are that the patient has (1) dementia, such that cognitive or behavioral symptoms (a) are interfering with the ability to function at work or usual activities, (b) represent a decline from previous level of functioning, (c) are not explained by delirium or major psychiatric disorder, (d) are detected and diagnosed, and (e) involve a minimum of two domains including memory, executive function, visuospatial abilities, language, and personality or behavior or comportment; (2) insidious onset; (3) clear-cut history of worsening of cognition; (4) prominent cognitive deficits by history and examination from either (a) an amnestic presentation or (b) a non-amnestic presentation, which can be a language, visuospatial, or executive dysfunction presentation; and lastly (5) no (a) substantial concomitant cerebrovascular disease, (b) core features of Dementia with Lewy Bodies, (c) prominent features of behavioral variant frontotemporal dementia (FTD), (d) prominent features of primary progressive aphasia, or (e) evidence for another concurrent, active disorder or use of medication that could have a substantial effect on cognition. All diagnoses are made by the BU ADRC clinical core consensus and confirmed by Dr. Budson. The majority of patients will have a positive AD biomarker, either from cerebrospinal fluid (CSF) or positron emission tomography (PET). See also Additional Inclusion/
Exclusion criteria
below. MCI due to AD. Meets MCI due to AD according to NIA-AA criteria 86; MoCA \>18 85; performance on Uniform Data Set version 3 (UDS-3) delayed recall (Craft Story 21) and recognition (Benson Complex Figure) memory worse than 1.0 SD for age and education adjusted norms. A summary of the NIA-AA criteria for MCI due to AD are that there is (1) clinical concern reflecting a change in cognition reported by patient, informant, or clinician; (2) objective impairment in one or more domains, typically including memory; (3) preservation of independence in functional abilities; (4) not demented; (5) a rule out of vascular, traumatic, and medical causes of cognitive decline; (6) evidence of longitudinal decline in cognition, when feasible; (7) history consistent with AD genetic factors, where relevant. All diagnoses are made by the BU ADRC clinical core consensus and confirmed by Dr. Budson. The majority of patients will have a positive AD biomarker, either from CSF or PET. See also Additional Inclusion/
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Memory performance (active stimulation condition) | Time Frame: Memory performance data is collected during active brain stimulation and reported 1 year later | The accuracy of task performance on memory test |
| Memory performance (sham stimulation condition) | Time Frame: Memory performance data is collected during sham brain stimulation and reported 1 year later | The accuracy of task performance on memory test |
Countries
United States
Contacts
Primary ContactRobert M. G. Reinhart, PhD
Outcome results
None listed