For mild neurocognitive disorder due to Alzheimers, probable Alzheimers disease can be diagnosed if there is genetic evidence, whereas possible Alzheimers disease can be met if all of the following are present: no genetic evidence, decline in both learning and memory, two or more cognitive deficits, and a functional disability not from another disorder.The NIA-AA criteria are used mainly in research rather than in clinical assessments. They define Alzheimers disease through three major stages: preclinical, mild cognitive impairment (MCI), and Alzheimers dementia. Diagnosis in the preclinical stage is complex and focuses on asymptomatic individuals; the latter two stages describe individuals experiencing symptoms. The core clinical criteria for MCI is used along with identification of biomarkers, predominantly those for neuronal injury (mainly tau-related) and amyloid beta deposition. The core clinical criteria itself rests on the presence of cognitive impairment without the presence of comorbidities. The third stage is divided into probable and possible Alzheimers disease dementia. In probable Alzheimers disease dementia there is steady impairment of cognition over time and a memory-related or non-memory-related cognitive dysfunction. In possible Alzheimers disease dementia, another causal disease such as cerebrovascular disease is present. Techniques
Neuropsychological tests including cognitive tests such as the Mini–Mental State Examination (MMSE), the Montreal Cognitive Assessment (MoCA) and the Mini-Cog are widely used to aid in diagnosis of the cognitive impairments in AD.
Likewise the hypothesis is, that as infants go through states of cognitive development, people with Alzheimers disease go through the reverse process of progressive cognitive impairment.The association with celiac disease is unclear, with a 2019 study finding no increase in dementia overall in those with CD, while a 2018 review found an association with several types of dementia including Alzheimers disease. Pathophysiology
Neuropathology
Alzheimers disease is characterised by loss of neurons and synapses in the cerebral cortex and certain subcortical regions. This loss results in gross atrophy of the affected regions, including degeneration in the temporal lobe and parietal lobe, and parts of the frontal cortex and cingulate gyrus. Degeneration is also present in brainstem nuclei particularly the locus coeruleus in the pons. Studies using MRI and PET have documented reductions in the size of specific brain regions in people with Alzheimers disease as they progressed from mild cognitive impairment to Alzheimers disease, and in comparison with similar images from healthy older adults.Both Aβ plaques and neurofibrillary tangles are clearly visible by microscopy in brains of those with Alzheimers disease, especially in the hippocampus. However, Alzheimers disease may occur without neurofibrillary tangles in the neocortex. Plaques are dense, mostly insoluble deposits of beta-amyloid peptide and cellular material outside and around neurons. Tangles (neurofibrillary tangles) are aggregates of the microtubule-associated protein tau which has become hyperphosphorylated and accumulate inside the cells themselves.