scispace - formally typeset
Search or ask a question
Author

David A. Drachman

Bio: David A. Drachman is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Dementia & Alzheimer's disease. The author has an hindex of 47, co-authored 134 publications receiving 38133 citations. Previous affiliations of David A. Drachman include Harvard University & Northwestern University.


Papers
More filters
Journal ArticleDOI
TL;DR: The criteria proposed are intended to serve as a guide for the diagnosis of probable, possible, and definite Alzheimer's disease; these criteria will be revised as more definitive information becomes available.
Abstract: Clinical criteria for the diagnosis of Alzheimer's disease include insidious onset and progressive impairment of memory and other cognitive functions. There are no motor, sensory, or coordination deficits early in the disease. The diagnosis cannot be determined by laboratory tests. These tests are important primarily in identifying other possible causes of dementia that must be excluded before the diagnosis of Alzheimer's disease may be made with confidence. Neuropsychological tests provide confirmatory evidence of the diagnosis of dementia and help to assess the course and response to therapy. The criteria proposed are intended to serve as a guide for the diagnosis of probable, possible, and definite Alzheimer's disease; these criteria will be revised as more definitive information become available.

26,847 citations

Journal ArticleDOI
TL;DR: Individuals of 50 years and older who were prescribed statins had a substantially lowered risk of developing dementia, independent of the presence or absence of untreated hyperlipidaemia, or exposure to nonstatin LLAs.

1,637 citations

Journal ArticleDOI
TL;DR: Comparisons of the memory and cognitive deficits induced by scopolamine with the performance of aged subjects revealed a marked similarity of pattern, and the possible theoretical explanations for the behavioral similarity seen with central cholinergic blockade and normal aging are discussed.
Abstract: The relationship of the cholinergic system of the brain to memory and cognitive functions was studied in human subjects by the use of scopolamine, methscopolamine bromide, and physostigmine. A battery of tests evaluated immediate memory span, memory storage (acquisition), and retrieval, as well as nonmemory cognitive ability. Subjects receiving scopolamine showed impairment of memory storage and possibly retrieval despite normal immediate memory span; nonmemory cognitive functions were also impaired. Neither methscopolamine (a peripherally acting scopolamine analogue) nor physostigmine (a centrally acting anticholinesterase agent) produced any significant changes in memory or other cognitive functions. Comparisons of the memory and cognitive deficits induced by scopolamine with the performance of aged subjects revealed a marked similarity of pattern. The possible theoretical explanations for the behavioral similarity seen with central cholinergic blockade and normal aging are discussed.

1,386 citations

Journal ArticleDOI
20 Feb 1987-Science
TL;DR: The chromosomal location of this defective gene has been discovered by using genetic linkage to DNA markers on chromosome 21 and provides an explanation for the occurrence of Alzheimer's disease-like pathology in Down syndrome.
Abstract: Alzheimer's disease is a leading cause of morbidity and mortality among the elderly. Several families have been described in which Alzheimer's disease is caused by an autosomal dominant gene defect. The chromosomal location of this defective gene has been discovered by using genetic linkage to DNA markers on chromosome 21. The localization on chromosome 21 provides an explanation for the occurrence of Alzheimer's disease-like pathology in Down syndrome. Isolation and characterization of the gene at this locus may yield new insights into the nature of the defect causing familial Alzheimer's disease and possibly, into the etiology of all forms of Alzheimer's disease.

1,158 citations

Journal ArticleDOI
TL;DR: Physostigmine, a pharmacologic antagonist of scopolamine, markedly improved M/C functions; amphetamine failed to produce M/ cognitive improvement, although alertness was improved, and activity in catecholaminergic neurons presumably increased, which supports a specific role for cholinergic neurons in M-C processes.
Abstract: Interference with cholinergic function produces disruption of memory/cognitive (M/C) performance in both animals and man. It is uncertain whether this disruption is due to a specific relation of cholinergic neurons to M/C functions, or whether the effect is nonspecific, resulting either from alteration of alertness and attention, or from a “mass action” effect, with loss of functioning neurons. Scopolamine was given to normal subjects to produce an M/C impairment. Half the test subjects then received physostigmine and half d-amphetamine. Physostigmine, a pharmacologic antagonist of scopolamine, markedly improved M/C functions; amphetamine failed to produce M/C improvement, although alertness was improved, and activity in catecholaminergic neurons presumably increased. This comparison supports a specific role for cholinergic neurons in M/C processes. Possible mechanisms of cholinergic neural functioning in memory include plasticity of cholinergic synapses, as well as other acetylcholine-depended operations of the limbic system crucial to memory.

641 citations


Cited by
More filters
Journal ArticleDOI
TL;DR: A 10‐minute cognitive screening tool (Montreal Cognitive Assessment, MoCA) to assist first‐line physicians in detection of mild cognitive impairment (MCI), a clinical state that often progresses to dementia.
Abstract: Objectives: To develop a 10-minute cognitive screening tool (Montreal Cognitive Assessment, MoCA) to assist first-line physicians in detection of mild cognitive impairment (MCI), a clinical state that often progresses to dementia. Design: Validation study. Setting: A community clinic and an academic center. Participants: Ninety-four patients meeting MCI clinical criteria supported by psychometric measures, 93 patients with mild Alzheimer's disease (AD) (Mini-Mental State Examination (MMSE) score≥17), and 90 healthy elderly controls (NC). Measurements: The MoCA and MMSE were administered to all participants, and sensitivity and specificity of both measures were assessed for detection of MCI and mild AD. Results: Using a cutoff score 26, the MMSE had a sensitivity of 18% to detect MCI, whereas the MoCA detected 90% of MCI subjects. In the mild AD group, the MMSE had a sensitivity of 78%, whereas the MoCA detected 100%. Specificity was excellent for both MMSE and MoCA (100% and 87%, respectively). Conclusion: MCI as an entity is evolving and somewhat controversial. The MoCA is a brief cognitive screening tool with high sensitivity and specificity for detecting MCI as currently conceptualized in patients performing in the normal range on the MMSE.

16,037 citations

Journal ArticleDOI
TL;DR: The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available.
Abstract: The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia. The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available. We present criteria for all-cause dementia and for AD dementia. We retained the general framework of probable AD dementia from the 1984 criteria. On the basis of the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis. We also retained the term possible AD dementia, but redefined it in a manner more focused than before. Biomarker evidence was also integrated into the diagnostic formulations for probable and possible AD dementia for use in research settings. The core clinical criteria for AD dementia will continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much work lies ahead for validating the biomarker diagnosis of AD dementia.

13,710 citations

Journal ArticleDOI
TL;DR: The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations, permitting the differentiation of six stages.
Abstract: Eighty-three brains obtained at autopsy from nondemented and demented individuals were examined for extracellular amyloid deposits and intraneuronal neurofibrillary changes. The distribution pattern and packing density of amyloid deposits turned out to be of limited significance for differentiation of neuropathological stages. Neurofibrillary changes occurred in the form of neuritic plaques, neurofibrillary tangles and neuropil threads. The distribution of neuritic plaques varied widely not only within architectonic units but also from one individual to another. Neurofibrillary tangles and neuropil threads, in contrast, exhibited a characteristic distribution pattern permitting the differentiation of six stages. The first two stages were characterized by an either mild or severe alteration of the transentorhinal layer Pre-alpha (transentorhinal stages I-II). The two forms of limbic stages (stages III-IV) were marked by a conspicuous affection of layer Pre-alpha in both transentorhinal region and proper entorhinal cortex. In addition, there was mild involvement of the first Ammon's horn sector. The hallmark of the two isocortical stages (stages V-VI) was the destruction of virtually all isocortical association areas. The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations.

13,699 citations

Journal ArticleDOI
19 Jul 2002-Science
TL;DR: It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid β-peptide in plaques in brain tissue and the rest of the disease process is proposed to result from an imbalance between Aβ production and Aβ clearance.
Abstract: It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer9s disease (AD) may be caused by deposition of amyloid β-peptide (Aβ) in plaques in brain tissue. According to the amyloid hypothesis, accumulation of Aβ in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Aβ production and Aβ clearance.

12,652 citations

Journal ArticleDOI
13 Aug 1993-Science
TL;DR: The APOE-epsilon 4 allele is associated with the common late onset familial and sporadic forms of Alzheimer9s disease (AD) in 42 families with late onset AD.
Abstract: The apolipoprotein E type 4 allele (APOE-epsilon 4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer9s disease (AD). Risk for AD increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE-epsilon 4 alleles in 42 families with late onset AD. Thus APOE-epsilon 4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE-epsilon 4 was virtually sufficient to cause AD by age 80.

8,669 citations